Comprehensive Physiology Wiley Online Library

Effect of Local Metabolic Factors on Vascular Smooth Muscle

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Oxygen
1.1 Effect
1.2 Mechanisms of Action
1.3 Situations in Which O2 Tension in Vessel Wall May Influence Vascular Tone
2 Potassium Ion
2.1 Effect
2.2 Mechanisms of Action
2.3 Situations in Which Vessel Wall [K+] May Influence Vascular Tone
3 Osmolarity
3.1 Effect
3.2 Mechanisms of Action
3.3 Situations in Which Changes in Tissue Vessel Wall Osmolarity May Influence Vascular Tone
Figure 1. Figure 1.

Change in canine vascular resistance (forelimb, kidney, and heart) and ventricular contractile force as a function of low arterial blood Po2. Arterial blood is passed through an isolated, ventilated lung. Graded changes in Po2 accomplished by altering gas mixture used to ventilate lung.

From Daugherty et al.
Figure 2. Figure 2.

Changes in perivascular Po2 caused by superfusing a hamster cheek pouch preparation with low (Po2 = 11 mmHg), intermediate (Po2 = 47 mmHg), and high (Po2 = 84 mmHg) Po2 solution. Hatched bars indicate changes observed when solution was changed from low to intermediate Po2; open bars indicate effect of changing from low to high Po2. Values are shown as means ± SE. Numbers in the bars are number of experiments performed. Asterisks indicate a significant difference was detected with Student's t test at 5% level of confidence.

From Duling , by permission of the American Heart Association, Inc
Figure 3. Figure 3.

Relation of Po2 to contractile tension developed by rabbit aortic strip in response to 3 μg/l epinephrine (Epi). Specific oxygen tensions are indicated by numbers on Po2 tracing.

From Detar and Bohr
Figure 4. Figure 4.

A: relation of critical solution Po2 to square of one‐half rabbit aortic strip thickness, a2. Each point represents one experiment. Least‐squares regression line is shown. B: relation of critical solution Po2 (P8c) to a′2. The a′ is a measure of strip thickness that takes into account width of strips. This offers another dimension for diffusion of O2. See Ref. for further explanation. Each point represents one experiment. Equation for least‐squares regression line and the correlation coefficient are given. These plots suggest that diffusion distance, a, is the primary variable influencing critical Po2 and that for a sufficiently thin strip the critical Po2 would be close to that of mitochondria. The point X is from Fay (.

From Pittman and Duling
Figure 5. Figure 5.

Effect of graded reductions in bath Po2 and increases in bath [CN] on oxygen consumption (2) and tension developments in rabbit aortic strips. A: active tension caused by norepinephrine. B: active tension caused by K+. Maximum oxygen uptake and tension development were not different for K+ and norepinephrine. Note that norepinephrine‐induced tension is much more sensitive to reductions in bath Po2 than is K+‐induced tension. Cyanide has less effect on tension for a given o2 than does Po2 when the agonist is norepinephrine. These results suggest that a factor other than oxidative phosphorylation is involved in response of rabbit aorta to lowered bath Po2, especially when tension is produced by norepinephrine.

From Coburn
Figure 6. Figure 6.

Isolated pulmonary arterial and aortic strips were incubated in a muscle bath at Po2 20 mmHg for 4 h. Epinephrine was then added to bath (vertical arrow). When bath Po2 was lowered to near zero, pulmonary strip contracted and aorta relaxed. Raising bath Po2 caused pulmonary strip to relax and aortic strip to contract.

From Detar and Gellai
Figure 7. Figure 7.

Skeletal muscle blood flow (MF) and venous Po2 when dogs were breathing 1 atm room air (control) compared with dogs breathing 100% oxygen under 2 atm pressure. Note that MF curve remains within control area. The venous Po2 curve, however, is well above, and is no longer similar in shape to its room‐air control, suggesting that in this case autoregulation of flow is not dependent on oxygen tension. ΔP is local perfusion pressure minus venous pressure.

From Bond et al.
Figure 8. Figure 8.

Autoregulatory response of skeletal muscle flow to reduction in perfusion pressure. A: under normal conditions. B: during mild hypoxia. Note smaller change in flow for a given decrease in pressure during mild hypoxia. This suggests that resistance vessels are sensitive to lowered tissue perfusion if tissue Po2 is sufficiently low. PA, iliac artery pressure; PV, iliac vein pressure; A‐V/ΔO2, arteriovenous oxygen difference; FA, iliac artery flow; o2,muscle oxygen uptake; Pvo2, iliac vein oxygen tension; Kf,capillary filtration coefficient.

From Granger et al. , by permission of the American Heart Association, Inc
Figure 9. Figure 9.

Relation between oxygen consumption and blood flow, □; venous Po2, ○; and venous hemoglobin saturation, Δ, of denervated canine skeletal muscle. Various O2 consumptions produced by twitch rates ranging from 0.25 to 8/s.

From Sparks
Figure 10. Figure 10.

Average time course of changes in coronary sinus O2 content and coronary vascular resistance. A: after a step increase in heart rate. B: after a step decrease in heart rate. To compare time courses of these two variables, it is necessary to take into account the delay and dispersion between capillary changes in O2 content and the venous measurement site. This was done by convoluting the changes in vascular resistance with dye curve estimates of venous transit, so that both coronary sinus O2 content and vascular resistance are subjected to the same delay and dispersion. When this is done, changes in coronary sinus O2 precede changes in coronary vascular resistance. Because flow was held constant, changes in oxygen consumption preceded changes in vascular resistance. *, Convolution integral has been applied to these data.

From Belloni and Sparks
Figure 11. Figure 11.

Model used to calculate arteriolar wall Po2 based on values for O2 flux across vascular wall, Jo2; permeability‐surface area product for O2 for the vessel wall, PS; Po2 within the vessel, Po2N and Po2 in tissue surrounding the arteriole, . Given flow through the vessel, F, and O2 content of blood, [O2]N‐1, the delivery of O2 into an arteriolar segment can be calculated. The exit of O2 from a segment is the sum of the flow removal, F[O2]N, and the flux across the wall, Jo2. Wall Po2 for any segment can be calculated from the resting Po2 gradient across the wall, Δ, and the ratio of the flux in a given condition, , to the resting O2 flux, . Values for most parameters and variables were taken from or derived from data supplied by Duling . Changes in flow and tissue Po2 were estimated from changes in flow and venous Po2 associated with exercise of canine skeletal muscles (see Fig. ).

Figure 12. Figure 12.

Results of simulated graded exercise using model in Figure . Flow and venous Po2 values were used as inputs. Average wall Po2, obtained by averaging the wall Po2's of each segment, decreases with small increases in oxygen consumption because the fall in tissue Po2, reflected by venous Po2, has more influence on wall Po2 than the increased flow delivery of O2. But once oxygen consumption is above ∼5 ml/min · 100 g the increased flow delivery of O2 dominates and arteriolar wall Po2 increases. The qualitative point is that arteriolar wall Po2 does not necessarily decrease during exercise because it is maintained by increased flow delivery of O2.

Figure 13. Figure 13.

Effects of 40 μmol isosmotic KCl injected into the circumflex coronary artery. A: effect on aortic blood pressure, heart rate, and mean circumflex blood flow. B: effect on aortic blood pressure and pulsatile circumflex blood flow. Increase in end‐diastolic flow (B) indicates that the increased flow is not the result of decreased ventricular force of contractions.

From Murray and Sparks , by permission of the American Heart Association, Inc
Figure 14. Figure 14.

Comparison of effects of KCl on response of rabbit aorta and mesoappendix ‘arteriole’ to epinephrine. Increase in bath [K+] from 4.7 mM to 10 mM caused contraction of aorta and relaxation of the smaller vessel.

From Bohr and Goulet
Figure 15. Figure 15.

Simultaneous records of contraction and 3H efflux during exposure to K+‐free physiologic saline solution (time enclosed by arrows). The 3H efflux was shown to represent efflux of [3H]norepinephrine. When K+ is replaced, relaxation precedes reduction in efflux of 3H. The washout delay of the system is shown by open circles, indicating that slower decrease in 3H efflux is not an artifact of washout. Because relaxation occurs faster than decrease in 3H release, it appears that relaxation is not the result of reduced norepinephrine release.

From Bonaccorsi et al.
Figure 16. Figure 16.

Actions of K+ concentration and Ba2+ on resting membrane potential (Em) and input resistance (rin). A: resting Em did not reach slope of 60 mV/decade in solutions with normal Cl and without Ba2+ (circles, solid line); slope was decreased by Ba2+ both in normal Cl (triangles, solid line) and in low Cl (squares, broken line) solutions. All lines extrapolate to a zero‐potential intercept of 160 mM. Standard errors for potential measurements were less than 2 mV and thus are not shown. B: rin decreased with higher [K+]o in all solutions. At lower [K+]o, Ba2+ increased rin in both normal and low [Cl]o solutions. Symbols reflect same solutions described in A. All curves are drawn by approximation. Standard errors are shown for normal solutions and solutions with Ba2+ and normal Cl, but not in solutions with low Cl to avoid confusion (n = 26–43 for each point). All measurements were made 2–10 min after a [K+]o change.

From Hermsmeyer
Figure 17. Figure 17.

Effect of increasing [K]o from 3.18 mM to 7.18 mM during agonist‐induced contractile response. A: coronary strips stimulated with acetylcholine. B: deep femoral arterial strips stimulated with norepinephrine. In both strips, potassium‐induced relaxation was followed by recovery of tension back to the prerelaxation level within 5 min. Tension reached a new steady‐state level above control in each strip.

From Gellai and Detar , by permission of the American Heart Association, Inc
Figure 18. Figure 18.

Average effects of prolonged heavy exercise of dog gracilis muscle on resistance (RDG), flow (FDG), Po2, pH, Pco2, [K+], and osmolality (Osm) of venous blood. Note that although flow remains elevated (dots above error bars indicate statistical significance when compared to control) and resistance remains decreased during the entire 1‐h stimulation period, venous [K+] and osmolarlity return to near starting values.

From Stowe et al.
Figure 19. Figure 19.

Time course of interstitial [K+], calculated from data in Reference , compared to time course of vascular conductance of skeletal muscle following a 1‐s period of tetanus at zero time. Change in interstitial [K+] precedes change in vascular conductance. This suggests that elevated [K+] is a cause of vasodilation that follows brief periods of tetanus.

Figure 20. Figure 20.

Tension and perfusion pressure (at constant flow) of isolated skeletal muscle preparations from a control dog and a dog depleted of K+ by dietary restriction. Note that muscle of K+‐depleted dog developed less tension and exhibited less vasodilation with elimination of second phase of initial vasodilator response. Circled numbers indicate phases of vasodilator response.

From Hazeyama and Sparks
Figure 21. Figure 21.

Left coronary artery blood flow of a dog was reduced in steps as indicated by number at top of figure. Change in coronary vascular resistance reaches a minimum value at 22 min, but K+ release began to dramatically increase only after that. This result suggests that K+ release does not play a role in autoregulation of coronary blood flow. Lactate refers to arterial and venous blood concentration of lactate. S‐T refers to changes in S‐T segment of electrocardiogram from isoelectric value.

From Case et al.
Figure 22. Figure 22.

Changes in arterial pressure (AP) and femoral flow (Q) of dog in response to intra‐arterial infusions of hypertonic sucrose, glucose, or urea. Note peak transit response which then returns toward control levels. Flow remains elevated in response to sucrose and glucose, but not to urea. Infusion began at ↑ and stopped at ↓.

From Stainsby and Barclay , by permission of the American Heart Association, Inc
Figure 23. Figure 23.

Effects of hyperosmotic solutions on spontaneous mechanical activity of rat portal vein. Period in hyperosmotic solution indicated by bar. Note that reduced frequency of contraction as well as reduced tension development are transient and in the case of urea, both variables return to base‐line values.

From Johansson and Jonsson
Figure 24. Figure 24.

Effect of hyperosmolarity on spontaneous contractions of rat portal vein. Period in hyperosmolar medium is indicated by bar. A: addition of 40 mmol NaCl/l medium. B: addition of 80 mmol sucrose/l medium. C: addition of 80 mmol urea/l medium. Note that initial reduction in rate and amplitude of contractions is soon replaced by elevated contractile force.

From McKinley et al.
Figure 25. Figure 25.

Diagram showing blood flow in cat skeletal muscle (ml/min‐100 g at perfusion pressure of 100 mmHg) during exercise and during intra‐arterial infusion of hypertonic solutions plotted against corresponding increases in venous osmolality. Note that for a given increase in venous osmolality the increase in steady‐state vascular conductance during infusion of hyperosmotic solutions is less than 50% of the increase in conductance observed during exercise.

From Lundvall
Figure 26. Figure 26.

Vascular resistance of dog skeletal muscle plotted as a function of venous osmolarity during exercise and infusion of hypertonic solutions. At both 1 and 5 min after initiation of exercise (indicated by 1 and 5), there is a relatively large decrease in resistance and little increase in venous osmolarity.

From Scott et al.


Figure 1.

Change in canine vascular resistance (forelimb, kidney, and heart) and ventricular contractile force as a function of low arterial blood Po2. Arterial blood is passed through an isolated, ventilated lung. Graded changes in Po2 accomplished by altering gas mixture used to ventilate lung.

From Daugherty et al.


Figure 2.

Changes in perivascular Po2 caused by superfusing a hamster cheek pouch preparation with low (Po2 = 11 mmHg), intermediate (Po2 = 47 mmHg), and high (Po2 = 84 mmHg) Po2 solution. Hatched bars indicate changes observed when solution was changed from low to intermediate Po2; open bars indicate effect of changing from low to high Po2. Values are shown as means ± SE. Numbers in the bars are number of experiments performed. Asterisks indicate a significant difference was detected with Student's t test at 5% level of confidence.

From Duling , by permission of the American Heart Association, Inc


Figure 3.

Relation of Po2 to contractile tension developed by rabbit aortic strip in response to 3 μg/l epinephrine (Epi). Specific oxygen tensions are indicated by numbers on Po2 tracing.

From Detar and Bohr


Figure 4.

A: relation of critical solution Po2 to square of one‐half rabbit aortic strip thickness, a2. Each point represents one experiment. Least‐squares regression line is shown. B: relation of critical solution Po2 (P8c) to a′2. The a′ is a measure of strip thickness that takes into account width of strips. This offers another dimension for diffusion of O2. See Ref. for further explanation. Each point represents one experiment. Equation for least‐squares regression line and the correlation coefficient are given. These plots suggest that diffusion distance, a, is the primary variable influencing critical Po2 and that for a sufficiently thin strip the critical Po2 would be close to that of mitochondria. The point X is from Fay (.

From Pittman and Duling


Figure 5.

Effect of graded reductions in bath Po2 and increases in bath [CN] on oxygen consumption (2) and tension developments in rabbit aortic strips. A: active tension caused by norepinephrine. B: active tension caused by K+. Maximum oxygen uptake and tension development were not different for K+ and norepinephrine. Note that norepinephrine‐induced tension is much more sensitive to reductions in bath Po2 than is K+‐induced tension. Cyanide has less effect on tension for a given o2 than does Po2 when the agonist is norepinephrine. These results suggest that a factor other than oxidative phosphorylation is involved in response of rabbit aorta to lowered bath Po2, especially when tension is produced by norepinephrine.

From Coburn


Figure 6.

Isolated pulmonary arterial and aortic strips were incubated in a muscle bath at Po2 20 mmHg for 4 h. Epinephrine was then added to bath (vertical arrow). When bath Po2 was lowered to near zero, pulmonary strip contracted and aorta relaxed. Raising bath Po2 caused pulmonary strip to relax and aortic strip to contract.

From Detar and Gellai


Figure 7.

Skeletal muscle blood flow (MF) and venous Po2 when dogs were breathing 1 atm room air (control) compared with dogs breathing 100% oxygen under 2 atm pressure. Note that MF curve remains within control area. The venous Po2 curve, however, is well above, and is no longer similar in shape to its room‐air control, suggesting that in this case autoregulation of flow is not dependent on oxygen tension. ΔP is local perfusion pressure minus venous pressure.

From Bond et al.


Figure 8.

Autoregulatory response of skeletal muscle flow to reduction in perfusion pressure. A: under normal conditions. B: during mild hypoxia. Note smaller change in flow for a given decrease in pressure during mild hypoxia. This suggests that resistance vessels are sensitive to lowered tissue perfusion if tissue Po2 is sufficiently low. PA, iliac artery pressure; PV, iliac vein pressure; A‐V/ΔO2, arteriovenous oxygen difference; FA, iliac artery flow; o2,muscle oxygen uptake; Pvo2, iliac vein oxygen tension; Kf,capillary filtration coefficient.

From Granger et al. , by permission of the American Heart Association, Inc


Figure 9.

Relation between oxygen consumption and blood flow, □; venous Po2, ○; and venous hemoglobin saturation, Δ, of denervated canine skeletal muscle. Various O2 consumptions produced by twitch rates ranging from 0.25 to 8/s.

From Sparks


Figure 10.

Average time course of changes in coronary sinus O2 content and coronary vascular resistance. A: after a step increase in heart rate. B: after a step decrease in heart rate. To compare time courses of these two variables, it is necessary to take into account the delay and dispersion between capillary changes in O2 content and the venous measurement site. This was done by convoluting the changes in vascular resistance with dye curve estimates of venous transit, so that both coronary sinus O2 content and vascular resistance are subjected to the same delay and dispersion. When this is done, changes in coronary sinus O2 precede changes in coronary vascular resistance. Because flow was held constant, changes in oxygen consumption preceded changes in vascular resistance. *, Convolution integral has been applied to these data.

From Belloni and Sparks


Figure 11.

Model used to calculate arteriolar wall Po2 based on values for O2 flux across vascular wall, Jo2; permeability‐surface area product for O2 for the vessel wall, PS; Po2 within the vessel, Po2N and Po2 in tissue surrounding the arteriole, . Given flow through the vessel, F, and O2 content of blood, [O2]N‐1, the delivery of O2 into an arteriolar segment can be calculated. The exit of O2 from a segment is the sum of the flow removal, F[O2]N, and the flux across the wall, Jo2. Wall Po2 for any segment can be calculated from the resting Po2 gradient across the wall, Δ, and the ratio of the flux in a given condition, , to the resting O2 flux, . Values for most parameters and variables were taken from or derived from data supplied by Duling . Changes in flow and tissue Po2 were estimated from changes in flow and venous Po2 associated with exercise of canine skeletal muscles (see Fig. ).



Figure 12.

Results of simulated graded exercise using model in Figure . Flow and venous Po2 values were used as inputs. Average wall Po2, obtained by averaging the wall Po2's of each segment, decreases with small increases in oxygen consumption because the fall in tissue Po2, reflected by venous Po2, has more influence on wall Po2 than the increased flow delivery of O2. But once oxygen consumption is above ∼5 ml/min · 100 g the increased flow delivery of O2 dominates and arteriolar wall Po2 increases. The qualitative point is that arteriolar wall Po2 does not necessarily decrease during exercise because it is maintained by increased flow delivery of O2.



Figure 13.

Effects of 40 μmol isosmotic KCl injected into the circumflex coronary artery. A: effect on aortic blood pressure, heart rate, and mean circumflex blood flow. B: effect on aortic blood pressure and pulsatile circumflex blood flow. Increase in end‐diastolic flow (B) indicates that the increased flow is not the result of decreased ventricular force of contractions.

From Murray and Sparks , by permission of the American Heart Association, Inc


Figure 14.

Comparison of effects of KCl on response of rabbit aorta and mesoappendix ‘arteriole’ to epinephrine. Increase in bath [K+] from 4.7 mM to 10 mM caused contraction of aorta and relaxation of the smaller vessel.

From Bohr and Goulet


Figure 15.

Simultaneous records of contraction and 3H efflux during exposure to K+‐free physiologic saline solution (time enclosed by arrows). The 3H efflux was shown to represent efflux of [3H]norepinephrine. When K+ is replaced, relaxation precedes reduction in efflux of 3H. The washout delay of the system is shown by open circles, indicating that slower decrease in 3H efflux is not an artifact of washout. Because relaxation occurs faster than decrease in 3H release, it appears that relaxation is not the result of reduced norepinephrine release.

From Bonaccorsi et al.


Figure 16.

Actions of K+ concentration and Ba2+ on resting membrane potential (Em) and input resistance (rin). A: resting Em did not reach slope of 60 mV/decade in solutions with normal Cl and without Ba2+ (circles, solid line); slope was decreased by Ba2+ both in normal Cl (triangles, solid line) and in low Cl (squares, broken line) solutions. All lines extrapolate to a zero‐potential intercept of 160 mM. Standard errors for potential measurements were less than 2 mV and thus are not shown. B: rin decreased with higher [K+]o in all solutions. At lower [K+]o, Ba2+ increased rin in both normal and low [Cl]o solutions. Symbols reflect same solutions described in A. All curves are drawn by approximation. Standard errors are shown for normal solutions and solutions with Ba2+ and normal Cl, but not in solutions with low Cl to avoid confusion (n = 26–43 for each point). All measurements were made 2–10 min after a [K+]o change.

From Hermsmeyer


Figure 17.

Effect of increasing [K]o from 3.18 mM to 7.18 mM during agonist‐induced contractile response. A: coronary strips stimulated with acetylcholine. B: deep femoral arterial strips stimulated with norepinephrine. In both strips, potassium‐induced relaxation was followed by recovery of tension back to the prerelaxation level within 5 min. Tension reached a new steady‐state level above control in each strip.

From Gellai and Detar , by permission of the American Heart Association, Inc


Figure 18.

Average effects of prolonged heavy exercise of dog gracilis muscle on resistance (RDG), flow (FDG), Po2, pH, Pco2, [K+], and osmolality (Osm) of venous blood. Note that although flow remains elevated (dots above error bars indicate statistical significance when compared to control) and resistance remains decreased during the entire 1‐h stimulation period, venous [K+] and osmolarlity return to near starting values.

From Stowe et al.


Figure 19.

Time course of interstitial [K+], calculated from data in Reference , compared to time course of vascular conductance of skeletal muscle following a 1‐s period of tetanus at zero time. Change in interstitial [K+] precedes change in vascular conductance. This suggests that elevated [K+] is a cause of vasodilation that follows brief periods of tetanus.



Figure 20.

Tension and perfusion pressure (at constant flow) of isolated skeletal muscle preparations from a control dog and a dog depleted of K+ by dietary restriction. Note that muscle of K+‐depleted dog developed less tension and exhibited less vasodilation with elimination of second phase of initial vasodilator response. Circled numbers indicate phases of vasodilator response.

From Hazeyama and Sparks


Figure 21.

Left coronary artery blood flow of a dog was reduced in steps as indicated by number at top of figure. Change in coronary vascular resistance reaches a minimum value at 22 min, but K+ release began to dramatically increase only after that. This result suggests that K+ release does not play a role in autoregulation of coronary blood flow. Lactate refers to arterial and venous blood concentration of lactate. S‐T refers to changes in S‐T segment of electrocardiogram from isoelectric value.

From Case et al.


Figure 22.

Changes in arterial pressure (AP) and femoral flow (Q) of dog in response to intra‐arterial infusions of hypertonic sucrose, glucose, or urea. Note peak transit response which then returns toward control levels. Flow remains elevated in response to sucrose and glucose, but not to urea. Infusion began at ↑ and stopped at ↓.

From Stainsby and Barclay , by permission of the American Heart Association, Inc


Figure 23.

Effects of hyperosmotic solutions on spontaneous mechanical activity of rat portal vein. Period in hyperosmotic solution indicated by bar. Note that reduced frequency of contraction as well as reduced tension development are transient and in the case of urea, both variables return to base‐line values.

From Johansson and Jonsson


Figure 24.

Effect of hyperosmolarity on spontaneous contractions of rat portal vein. Period in hyperosmolar medium is indicated by bar. A: addition of 40 mmol NaCl/l medium. B: addition of 80 mmol sucrose/l medium. C: addition of 80 mmol urea/l medium. Note that initial reduction in rate and amplitude of contractions is soon replaced by elevated contractile force.

From McKinley et al.


Figure 25.

Diagram showing blood flow in cat skeletal muscle (ml/min‐100 g at perfusion pressure of 100 mmHg) during exercise and during intra‐arterial infusion of hypertonic solutions plotted against corresponding increases in venous osmolality. Note that for a given increase in venous osmolality the increase in steady‐state vascular conductance during infusion of hyperosmotic solutions is less than 50% of the increase in conductance observed during exercise.

From Lundvall


Figure 26.

Vascular resistance of dog skeletal muscle plotted as a function of venous osmolarity during exercise and infusion of hypertonic solutions. At both 1 and 5 min after initiation of exercise (indicated by 1 and 5), there is a relatively large decrease in resistance and little increase in venous osmolarity.

From Scott et al.
References
 1. Altura, B. M., and B. T. Altura. Differential effects of anoxia, exogenous glucose, and metabolic inhibitors on drug‐and hormone‐induced contractions of arterial smooth muscle. Circulatory Shock 3: 169–189, 1976.
 2. Altura, B. M., D. Malaviya, C. F. Reich, and L. R. Orkin. Effects of vasoactive agents on isolated human umbilical arteries and veins. Am. J. Physiol. 222: 345–355, 1972.
 3. Anderson, D. K. Cell potential and the sodium‐potassium pump in vascular smooth muscle. Federation Proc. 35: 1294–1297, 1976.
 4. Anderson, D. K., S. A. Roth, R. A. Brace, D. Radawski, F. J. Haddy, and J. B. Scott. Effect of hypokalemia and hypomagnesemia produced by hemodialysis on vascular resistance in canine skeletal muscle. Circulation Res. 31: 165–173, 1972.
 5. Andersson, C., P. Hellstrand, B. Johansson, and A. Ringberg. Contraction in venous smooth muscle induced by hypertonicity. Calcium dependence and mechanical characteristics. Acta Physiol. Scand. 90: 451–461, 1974.
 6. Avrill, A., B. Johansson, and O. Jonsson. Effects of hyperosmolarity on the volume of vascular smooth muscle cells and the relation between cell volume and muscle activity. Acta Physiol. Scand. 75: 484–495, 1969.
 7. Axelsson, J., B. Wahlström, B. Johansson, and O. Jonsson. Influence of the ionic environment on spontaneous electrical and mechanical activity of the rat portal vein. Circulation Res. 21: 609–618, 1967.
 8. Bachofen, M., A. Gage, and H. Bachofen. Vascular response to changes in blood oxygen tension under various blood flow rates. Am. J. Physiol. 220: 1786–1792, 1971.
 9. Barcroft, H. An enquiry into the nature of the mediator of the vasodilation in skeletal muscle in exercise and during circulatory arrest. J. Physiol. London 222: 99P–118P, 1972.
 10. Bates, D., and T. M. Sundt, Jr. The relevance of peripheral baroreceptors and chemoreceptors to regulation of cerebral blood flow in the cat. Circulation Res. 38: 488–493, 1976.
 11. Beaty, O., III, and D. E. Donald. Role of potassium in the transient reduction in vascoconstrictive responses of muscle resistance vessels during rhythmic exercise in dogs. Circulation Res. 41: 452–460, 1977.
 12. Belloni, F. L., and H. V. Sparks. Dynamics of myocardial oxygen consumption and coronary vascular resistance. Am. J. Physiol. 233: H34–H43, 1977 or
 13. Am. J. Physiol.: Heart Circ. Physiol. 2: H34–H43, 1977.
 14. Benumof, J. L., J. M. Mathers, and E. A. Wahrenbrock. Cyclic hypoxic pulmonary vasoconstriction induced by concomitant carbon dioxide changes. J. Appl. Physiol. 41: 466–469, 1976.
 15. Berne, R. M., J. R. Blackmon, and T. H. Gardner. Hypoxemia and coronary blood flow. J. Clin. Invest. 36: 1101–1106, 1957.
 16. Beven, J. A., and J. V. Osher. Effect of potassium on the resting length of vascular smooth muscle of the rabbit aorta and its response to l‐norepinephrine. Circulation Res. 13: 346–351, 1963.
 17. Biamino, G., and H. J. Wessel. Potassium induced relaxation of vascular smooth muscle: a possible mechanism of exercise hyperemia. Pfluegers Arch. European J. Physiol. 343: 95–106, 1973.
 18. Bicher, H. I. Brain oxygen autoregulation: a protective reflex to hypoxia? Microvascular Res. 8: 291–313, 1974.
 19. Bicher, H. I., and P. Marvin. Pharmacological control of local oxygen regulation mechanisms in brain tissue. Stroke 7: 469–472, 1976.
 20. Binet, L., and M. Burstein. Sur Taction vasoconstrictrice du serum sale hypertonique au niveau de la petite circulation. Compt. Rend. Soc. Biol. 145: 1766–1770, 1951.
 21. Bito, L. Z., and R. E. Meyers. On the physiological response of the cerebral cortex to acute stress (reversible asphyxia). J. Physiol. London 221: 349–379, 1972.
 22. Blaustein, M. P. Sodium ions, calcium ions, blood pressure regulation and hypertension: a reassessment and a hypothesis. Am. J. Physiol. 232: C165–C173, 1977 or
 23. Am. J. Physiol.: Cell Physiol. 1: C165–C173, 1977.
 24. Bockman, E. L., R. M. Berne, and R. Rubio. Release of adenosine and lack of release of ATP from contracting skeletal muscles. Pfluegers Arch. European J. Physiol. 355: 229–241, 1975.
 25. Bohr, D. F. Vascular Smooth Muscle. In: Peripheral Circulation, edited by P. C. Johnson. New York: Wiley, 1978, p. 13–44.
 26. Bohr, D. F., and P. L. Goulet. Role of electrolysis in the contractile machinery of vascular smooth muscle. Am. J. Cardiol. 8: 549–556, 1961.
 27. Bonaccorsi, A., K. Hermsmeyer, O. Aprighano, C. B. Smith, and D. F. Bohr. Mechanism of potassium relaxation in arterial muscle. Blood Vessels 14: 261–276, 1977.
 28. Bonaccorsi, A., K. Hermsmeyer, C. B. Smith, and D. F. Bohr. Norepinephrine release in isolated arteries induced by K+‐free solution. Am. J. Physiol. 232: H140–H145, 1977 or
 29. Am. J. Physiol.: Heart Circ. Physiol. 1: H140–H145, 1977.
 30. Bond, R. F., R. F. Blackard, and J. A. Taxis. Evidence against oxygen being the primary factor governing autoregulation. Am. J. Physiol. 216: 788–793, 1969.
 31. Bourdeau‐Martini, J., and C. R. Honig. Control of intercapillary distance in rat heart; effect of arterial pCO2 and pH. Microvascular Res. 6: 286–296, 1973.
 32. Bourdeau‐Martini, J., L. L. Odoroff, and C. R. Honig. Dual effect of oxygen on magnitude and uniformity of coronary intercapillary distance. Am. J. Physiol. 226: 800–810, 1974.
 33. Brace, R. A. Time course and mechanisms of the acute effects of hypokalemia and hyperkalemia on vascular resistance. Proc. Soc. Exptl. Biol. Med. 145: 1389–1394, 1974.
 34. Brace, R. A., and D. K. Anderson. Predicting transient and steady‐state changes in resting membrane potential. J. Appl. Physiol. 35: 90–94, 1973.
 35. Brace, R. A., D. K. Anderson, W. Chen, J. B. Scott, and F. J. Haddy. Local effects of hypokalemia on coronary resistance and myocardial contractile force. Am. J. Physiol. 227: 590–597, 1974.
 36. Brace, R. A., J. B. Scott, W. Chen, D. K. Anderson, and F. S. Haddy. Direct effects of hypoosmolality on vascular resistance and myocardial contractile force. Proc. Soc. Exptl. Biol. Med. 148: 578–583, 1975.
 37. Brecht, K., P. Konold, and G. Gebert. The effect of potassium, catecholamines and other vasoactive agents on isolated arterial segments of the muscular type. Physiol. Bohemoslov. 18: 15–22, 1969.
 38. Bünger, R., F. J. Haddy, A. Querengasser, and E. Gerlach. Studies on potassium induced coronary dilation in the isolated guinea pig heart. Pfluegers Arch. European J. Physiol. 363: 27–31, 1976.
 39. Burcher, E., and D. Garlick. Effects of exercise metabolites on adrenergic vasoconstriction in the gracilis muscle of the dog. J. Pharmacol. Exptl. Therap. 192: 149–156, 1975.
 40. Cameron, I. R., and J. Caronna. The effect of local changes in potassium and bicarbonate concentration on hypothalamic blood flow in the rabbit. J. Physiol. London 262: 415–430, 1976.
 41. Carlson, E. L., and H. V. Sparks. Intrarenal distribution of blood flow during elevation of ureteral pressure. Circulation Res. 26: 601–610, 1970.
 42. Carrier, O., and S. Shibata (editors). Factors Influencing Vascular Reactivity. New York: Igaku‐Shoin, 1977.
 43. Carrier, O.Jr., J. R. Walker, and A. C. Guyton. Role of oxygen in autoregulation of blood flow in isolated vessels. Am. J. Physiol. 206: 951–954, 1964.
 44. Case, R. B., M. G. Nasser, and R. Crampton. Biochemical aspects of early myocardial ischemia. Am. J. Cardiol. 24: 766–775, 1969.
 45. Chalmers, J. P., and P. I. Korner. Effect of arterial hypoxia on the cutaneous circulation of the rabbit. J. Physiol. London 184: 685–697, 1966.
 46. Chen, W. T., R. A. Brace, J. B. Scott, D. K. Anderson, and F. J. Haddy. The mechanism of the vasodilator action of potassium. Proc. Soc. Exptl. Biol. Med. 140: 820–824, 1972.
 47. Childs, C. M., K. E. Arfors, R. Tuma, and F. N. McKenzie. Continuous capillary red cell velocity measurements in the tenuissimus muscle under changing local oxygen tensions. Bibliotheca Anat. 13: 153–154, 1975.
 48. Chou, C. C., T. D. Burns, C. P. Hsieh, and J. B. Dabney. Mechanisms of local vasodilation with hypertonic glucose in the jejunum. Surgery 71: 380–387, 1972.
 49. Coburn, R. F. Oxygen tension sensors in vascular smooth muscle. In: Tissue Hypoxia and Ischemia, edited by M. Reivich, R. F. Coburn, S. Lahiri, and B. Chance. New York: Plenum, 1977, p. 101–115.
 50. Coburn, R. F., F. G. Ploegmakers, P. Gondrie, and R. Abboud. Myocardial myoglobin oxygen tension. Am. J. Physiol. 224: 870–876, 1973.
 51. Cohen, S. E. The influence of the Ca and K ions on toners and adrenaline response of the coronary arteries. Arch. Intern. Pharmacodyn. 54: 1–16, 1936.
 52. Cook, B. H., H. J. Granger, and A. E. Taylor. Metabolism of coronary arteries and arterioles. A histochemical study. Microvascular Res. 14: 145–160, 1977.
 53. Crawford, D. G., H. M. Fairchild, and A. C. Guyton. Oxygen lack as a possible cause of reactive hyperemia. Am. J. Physiol. 197: 613–616, 1959.
 54. Daniell, H. B., and E. E. Bagwell. Effects of high oxygen on coronary flow and heart force. Am. J. Physiol. 214: 1454–1459, 1968.
 55. Daugherty, R. M.Jr., J. B. Scott, J. M. Dabney, and F. J. Haddy. Local effects of O2 and CO2 on limb, renal and coronary vascular resistances. Am. J. Physiol. 213: 1102–1110, 1967.
 56. Daugherty, R. M.Jr., J. B. Scott, and F. J. Haddy. Effects of generalized hypoxemia and hypercapnia on forelimb vascular resistance. Am. J. Physiol. 213: 1111–1114, 1967.
 57. Dawes, G. S. The vasodilator action of K+. J. Physiol. London 99: 224–238, 1941.
 58. Dennis, J., and R. M. Moore. Potassium changes in the functioning heart under conditions of ischemia and of congestion. Am. J. Physiol. 123: 443–447, 1938.
 59. Detar, R., and D. F. Bohr. Oxygen and vascular smooth muscle contraction. Am. J. Physiol. 214: 241–244, 1968.
 60. Detar, R., and D. F. Bohr. Contractile responses of isolated vascular smooth muscle during prolonged exposure to anoxia. Am. J. Physiol. 222: 1269–1277, 1972.
 61. Detar, R., and M. Gellai. Oxygen and isolated vascular smooth muscle from the main pulmonary artery of the rabbit. Am. J. Physiol. 221: 1791–1794, 1971.
 62. Dornhorst, A. C., and R. F. Whelan. The blood flow in muscle following exercise and circulatory arrest: the influence of reduction in effective local blood pressure of arterial hypoxia and of adrenaline. Clin. Sci. 12: 33–40, 1953.
 63. Duling, B. R. Microvascular responses to alterations in oxygen tension. Circulation Res. 31: 481–489, 1972.
 64. Duling, B. R. Oxygen sensitivity of vascular smooth muscle. II. In vivo studies. Am. J. Physiol. 227: 42–49, 1974.
 65. Duling, B. R. Effects of potassium ion on the microcirculation of the hamster. Circulation Res. 37: 325–330, 1975.
 66. Duling, B. R., and R. M. Berne. Propagated vasodilation in the microcirculation of the hamster cheek pouch. Circulation Res. 26: 163–170, 1970.
 67. Duling, B. R., and R. M. Berne. Longitudinal gradients in periarteriolar oxygen tension. Circulation Res. 27: 669–678, 1970.
 68. Duling, B. R., and R. M. Berne. Oxygen and the local regulation of blood flow: possible significance of longitudinal gradients in arterial blood oxygen tension. Circulation Res. 28: (Suppl. 1) 65–69, 1971.
 69. Duling, B. R., and R. N. Pittman. Oxygen tension: dependent or independent variable in local control of blood flow? Federation Proc. 34: 2020–2024, 1975.
 70. Duling, B. R., and E. Staples. Microvascular effects of hypertonic solutions in the hamster. Microvascular Res. 11: 51–56, 1976.
 71. Eckenhoff, J. E., J. H. Hafkenschiel, C. M. Landmesser, and M. Harmel. Cardiac oxygen metabolism and control of the coronary circulation. Am. J. Physiol. 149: 634–649, 1947.
 72. Eklund, B. Influence of work duration on the regulation of muscle blood flow. Acta Physiol. Scand. Suppl. 92: (Suppl. 411) 2–64, 1974.
 73. Eklund, B., and L. Kaijser. Forearm blood flow after isometric contraction at different loads in relation to potentially vasodilating substances. Scand. J. Clin. Lab. Invest. 34: 23–29, 1974.
 74. Eliakim, M., S. Z. Rosenberg, and K. Braun. Effect of hypertonic saline on the pulmonary and systemic pressures. Circulation Res. 6: 357–362, 1958.
 75. Eliakim, M., S. Stern, and H. Nathan. Site of action of hypertonic saline in the pulmonary circulation. Circulation Res. 9: 327–332, 1961.
 76. Emanuel, D. A., J. B. Scott, and F. J. Haddy. Effect of potassium on small and large blood vessels of the dog forelimb. Am. J. Physiol. 197: 637–642, 1959.
 77. Even, P., F. Dray, F. Ruff, R. Durouc, M. C. Santais, and H. Sors. Measurement of prostaglandins E1, E2, and F2a, histamine and serotonin, upstream and downstream the lung during pulmonary vasopressor response to hypoxia in man. Effects of prostaglandin synthesis inhibitors. In: Lung Metabolism: Proteolysis and Antiproteolysis, Biochemical Pharmacology, Handling of Bioactive Substances, edited by A. Junod and A. DeHaller. New York: Academic, 1975, p. 365–385.
 78. Fairchild, H. M., J. Ross, and A. C. Guyton. Failure of recovery from reactive hyperemia in the absence of oxygen. Am. J. Physiol. 210: 490–492, 1966.
 79. Fay, F. S. Guinea pig ductus arteriosus. I. Cellular and metabolic basis for oxygen sensitivity. Am. J. Physiol. 221: 470–479, 1971.
 80. Fay, F. S., and F. F. Jöbsis. Guinea pig ductus arteriosus. III. Light absorption changes during response to O2. Am. J. Physiol. 223: 588–595, 1972.
 81. Fay, F. S., P. Nair, and W. J. Whalen. Mechanism of oxygen induced contraction of ductus arteriosus. In: Tissue Hypoxia and Ischemia, edited by M. Reivich, R. F. Coburn, S. Lahiri, and B. Chance. New York: Plenum, 1977, p. 123–133.
 82. Fenn, W. O. Loss of potassium in voluntary contraction. Am. J. Physiol. 120: 675–680, 1937.
 83. Fishman, A. P. Hypoxia on the pulmonary circulation. Circulation Res. 38: 221–231, 1976.
 84. Fishman, A. P. The sensing of oxygen tension in the pulmonary circulation. In: Tissue Hypoxia and Ischemia, edited by M. Reivich, R. F. Coburn, S. Lahiri, and B. Chance, New York: Plenum, 1977, p. 143–150.
 85. Fleisch, J. H. Pharmacology of the aorta. Blood Vessels 11: 193–205, 1974.
 86. Forbes, H. S., and G. I. Nason. The cerebral circulation. Vascular responses to (A) hypertonic solutions and (B) withdrawal of cerebrospinal fluid. Arch. Neurol. Psychiat. 34: 533–547, 1935.
 87. Freed, S. C., and A. M. Meunier. Effect of hypoxia on arterial muscle tone. Angiology 23: 1–6, 1972.
 88. Friedman, S. M., and C. L. Friedman. The action of ouabain on the smooth muscle cells of the rat tail artery. Proc. Soc. Exptl. Biol. Med. 146: 825–830, 1974.
 89. Friedman, S. M., M. Nakashiona, V. Palaty, and B. K. Walters. Vascular resistance and Na+‐K+ gradients in the perfused rat tail artery. Can. J. Physiol. Pharmacol. 51: 410–417, 1973.
 90. Furchgott, R. F. Discussion on the biochemistry of the arterial wall. Bibliotheca Cardiol. 15: 20–23, 1964.
 91. Gazitúa, S., J. B. Scott, C. C. Chou, and F. J. Haddy. Effect of osmolarity on canine renal vascular resistance. Am. J. Physiol. 217: 1216–1223, 1969.
 92. Gazitùa, S., J. B. Scott, B. Swindall, and F. J. Haddy. Resistance responses to local changes in plasma osmolality in three vascular beds. Am. J. Physiol. 220: 384–391, 1971.
 93. Gebert, G. Measurement of K+ and Na+ activity in the extracellular space of rabbit skeletal muscle during muscular work by means of glass microelectrodes. Pfluegers Arch. European J. Physiol. 331: 204–214, 1972.
 94. Gebert, G., and H. Piechowiak. Effect of potassium and norepinephrine on the tone of the isolated artery: changes by ouabain pretreatment. Experientia 30: 46–47, 1974.
 95. Gellai, M., and R. Detar. Evidence in support of hypoxia but against high potassium and hyper osmolarity as possible mediators of sustained vasodilation in rabbit cardiac and skeletal muscle. Circulation Res. 35: 681–691, 1974.
 96. Gellai, M., J. M. Norton, and R. Detar. Evidence for direct control of coronary vascular tone by oxygen. Circulation Res. 32: 279–289, 1973.
 97. Gerlings, E. D., D. T. Miller, and J. P. Gilmore. Oxygen availability: a determinant of myocardial potassium balance. Am. J. Physiol. 216: 559–562, 1969.
 98. Gillman, R. G., and A. C. Burton. Constriction of the neonatal aorta by raised oxygen tension. Circulation Res. 19: 755–765, 1966.
 99. Gilmore, J. P., and E. D. Gerlings. Influence of developed tension on myocardial potassium balance in the dog heart. Circulation Res. 22: 769–775, 1968.
 100. Gilmore, J. P., and E. D. Gerlings. Influence of interstimulus interval on myocardial potassium balance. Am. J. Physiol. 217: 136–141, 1969.
 101. Gilmore, J. P., J. A. Nizolek, Jr., and R. J. Jacob. Further characterization of myocardial K+ loss induced by changing contraction frequency. Am. J. Physiol. 221: 465–469, 1971.
 102. Gorczynski, R. J., and B. R. Duling. The role of O2 lack in contraction induced arteriolar vasodilation in hamster striated muscle. Federation Proc. 35: 448, 1976.
 103. Granger, H. J., A. H. Goodman, and B. H. Cook. Metabolic models of microcirculatory regulation. Federation Proc. 34: 2025–2030, 1975.
 104. Granger, H. J., A. H. Goodman, and O. N. Granger. Role of resistance and exchange vessels in local microvascular control of skeletal muscle oxygenation in the dog. Circulation Res. 38: 379–385, 1976.
 105. Granger, H. J., and A. P. Shepherd. Intrinsic microvascular control of tissue oxygen delivery. Microvascular Res. 5: 49–72, 1973.
 106. Gray, S. D. Effect of hypertoxicity on vascular dimensions in skeletal muscle. Microvascular Res. 3: 117–124, 1971.
 107. Griesemeyer, E. C., and L. A. Coret. “Recovery” responses of hypoxic arterial smooth muscle. J. Pharmacol. Exptl. Therap. 130: 294–302, 1960.
 108. Gurevich, M. I., S. A. Berhtein, and I. R. Evdokimov. The effect of changes in osmolarity and oxygen tension on excitability and conduction of excitation in vascular smooth muscles. In: Physiology of Smooth Muscle, edited by E. Bülbring and M. F. Shuba. New York: Raven, 1976, p. 153–161.
 109. Guyton, A. C., J. M. Ross, O. Carrier, Jr., and J. R. Walker. Evidence for tissue oxygen demand as the major factor causing autoregulation. Circulation Res. 14: (Suppl. 1) 60–68, 1964.
 110. Guz, A., G. S. Kurland, and A. S. Freedberg. Relation of coronary flow to oxygen supply. Am. J. Physiol. 199: 179–182, 1960.
 111. Haas, F., and E. H. Bergofsky. Role of the mast cell in the pulmonary pressor response to hypoxia. J. Clin. Invest. 51: 3154–3162, 1972.
 112. Haddy, F. J. Potassium and blood vessels. Life Sci. 16: 1489–1498, 1975.
 113. Haddy, F. J., and J. B. Scott. Metabolic factors in peripheral circulatory regulation. Federation Proc. 34: 2006–2011, 1975.
 114. Haddy, F. J., J. B. Scott, M. A. Florio, R. M. Daugherty, Jr., and J. N. Huizenga. Local vascular effects of hypokalemia, alkalosis, hypercalcemia, and Hypomagnesemia. Am. J. Physiol. 204: 202–212, 1963.
 115. Hales, C. A., E. Rouse, I. A. Buchwald, and H. Kazemi. Role of prostaglandins in alveolar hypoxic vasoconstriction. Respiration Physiol. 29: 151–162, 1977.
 116. Haljamäe, H., B. Johansson, O. Jonsson, and H. Röckert. The distribution of sodium, potassium and chloride in the smooth muscle of the rat portal vein. Acta Physiol. Scand. 78: 255–268, 1970.
 117. Hansen, A. K. The potassium concentration in cerebrospinal fluid in young and adult rats following complete brain ischemia. Effects of pretreatment with hypoxia. Acta Physiol. Scand. 97: 519–572, 1976.
 118. Harris, P. D., D. E. Longnecker, F. N. Miller, and D. L. Wiegman. Sensitivity of small subcutaneous vessels to altered respiratory gases and local pH. Am. J. Physiol. 231: 244–251, 1976.
 119. Harvey, R. B. Vascular resistance changes produced by hyperosmotic solutions. Am. J. Physiol. 199: 31–34, 1960.
 120. Hauge, A. Role of histamine in hypoxic pulmonary hypertension in the rat. I. Blockade or potentiation of endogenous amines, kinins, and ATP. Circulation Res. 22: 371–383, 1968.
 121. Hauge, A., and G. Bø. Blood hyper osmolarity and pulmonary vascular resistance in the cat. Circulation Res. 28: 371–376, 1971.
 122. Hauge, A., and K. L. Melmon. Role of histamine in hypoxic pulmonary hypertension in the rat. II. Depletion of histamine, serotonin, and catecholamines. Circulation Res. 22: 385–392, 1968.
 123. Hauge, A., and N. C. Staub. Prevention of hypoxic vasoconstriction in cat lung by histamine‐releasing agent 48/80. J. Appl. Physiol. 26: 693–699, 1969.
 124. Hazeyama, Y., and H. V. Sparks. Exercise hyperemia in potassium depleted dogs. Am. J. Physiol. 236: H480–H486, 1979 or
 125. Am. J. Physiol.: Heart Circ. Physiol. 5: H480–H486, 1979.
 126. Hazeyama, Y., and H. V. Sparks. A model of potassium ion efflux during exercise of skeletal muscle. Am. J. Physiol. 236: R83–R90, 1979 or
 127. Am. J. Physiol.: Regulative, Integrative Comp. Physiol. 5: R83–R90, 1979.
 128. Heistad, D. D., and F. M. Abboud. Factors that influence blood flow in skeletal muscle and skin. Anesthesiology 41: 139–156, 1974.
 129. Heistad, D. D., and M. L. Marcus. Controversies in cardiovascular research: evidence that neural mechanisms do not have important effects on cerebral blood flow. Circulation Res. 42: 295–302, 1978.
 130. Heistad, D. D., M. L. Marcus, J. C. Ehrhardt, and F. M. Abboud. Effect of stimulation of carotid chemoreceptors on total and regional cerebral blood flow. Circulation Res. 38: 20–25, 1976.
 131. Hellstrand, P. Oxygen consumption and lactate production of the rat portal vein in relation to its contractile activity. Acta Physiol. Scand. 100: 91–106, 1977.
 132. Hellstrand, P., B. Johansson, and K. Norberg. Mechanical, electrical and biochemical effects of hypoxia and substrate removal of spontaneously active vascular smooth muscle. Acta Physiol. Scand. 100: 69–83, 1977.
 133. Hendrickx, H., and R. Casteels. Electrogenic sodium pump in arterial smooth muscle cells. Pfluegers Arch. European J. Physiol. 346: 299–306, 1974.
 134. Henquell, L., and C. R. Honig. Intercapillary distances and capillary reserve in right and left ventricles: significance for control of tissue pO2. Microvascular Res. 12: 35–41, 1976.
 135. Henquell, L., and C. R. Honig. Capillary spacing around coronary venules suggests that diffusion distance is controlled by local tissue pO2. Microvascular Res. 15: 363–366, 1978.
 136. Herlihy, J. T., and R. A. Murphy. Absence of a direct effect of phosphate or 5′ AMP on the contractile proteins of hog arteries. Circulation Res. 28: 434–439, 1971.
 137. Hermsmeyer, K. Ba2+ and K+ alteration of K+ conductance in spontaneously active vascular muscle. Am. J. Physiol. 230: 1031–1036, 1976.
 138. Heuser, D., V. Knabes, G. Gebert, and E. Betz. Reactions of pial vessels during variation of local perivascular ionic composition of the CSF. European Neurol. 6: 96–99, 1971.
 139. Hilton, R., and F. Eichholtz. The influence of chemical factors in the coronary circulation. J. Physiol. London 59: 413–425, 1924.
 140. Hilton, S. M. A peripheral arterial conducting system underlying dilation of femoral artery and concerned with functional dilation in skeletal muscle. J. Physiol. London 149: 93–111, 1959.
 141. Hník, P., M. Holas, I. Krekule, N. Kříž, J. Mejsnar, V. Smieško, E. Ujec, and F. Vyskočil. Work‐induced potassium changes in skeletal muscle and effluent venous blood assessed by liquid ion‐exchanger microelectrodes. Pfluegers Arch. European J. Physiol. 362: 85–94, 1976.
 142. Hník, P., N. Kříž, F. Vyskočil, V. Smieško, J. Mejsnar, E. Ujec, and M. Holas. Work‐induced potassium changes in muscle venous effluent blood measured by ion‐specific electrodes. Pfluegers Arch. European J. Physiol. 28: 177–181, 1973.
 143. Hoff, J. T., E. T. Mackenzie, and A. M. Harper. Responses of the cerebral circulation to hypercapnia and hypoxia after 7th cranial nerve transection in baboons. Circulation Res. 40: 258–262, 1977.
 144. Honig, C. R. Control of smooth muscle actomyosin by phosphate and 5′AMP: possible role in metabolic autoregulation. Microvascular Res. 1: 133–146, 1968.
 145. Honig, C. R., and J. Bourdeau‐Martini. Extra‐vascular component of O2 transport in normal hypertrophic heart with special reference to O2 therapy. Circulation Res. 35: (Suppl. II) 97–103, 1974.
 146. Horstman, D. H., M. Gleser, and J. Delehunt. Effects of altering O2 delivery on Vo2 of isolated, working muscle. Am. J. Physiol. 230: 327–334, 1976.
 147. Hughes, M. J., and I. A. Coret. Evolution of epinephrine responses of hypoxic rabbit aortic muscle. Am. J. Physiol. 216: 1423–1428, 1969.
 148. Järhult, J. Osmolar control of the circulation in hemorrhagic hypotension. An experimental study in the cat. Acta Physiol. Scand. 94: (Suppl. 423) 1–84, 1975.
 149. Järhult, J., J. Hellman, and S. Mellander. Circulatory effects evoked by “physiological” increases of arterial osmolality. Acta Physiol. Scand. 93: 129–134, 1975.
 150. Jöbsis, F. F. Oxidative metabolism at low Po2. Federation Proc. 31: 1404–1413, 1972.
 151. Jöbsis, F. F. Intracellular metabolism of oxygen. Am. Rev. Respirat. Diseases 110 (part 2): 58–63, 1974.
 152. Jöbsis, F. F. What is a molecular oxygen sensor? What is a transduction process? In: Tissue Hypoxia and Ischemia, edited by M. Reivich, R. Coburn, S. Lahiri, and B. Chance. New York: Plenum, 1977, p. 3–17.
 153. Johansson, B. Processes involved in vascular smooth muscle contraction and relaxation. Circulation Res. 43: (Suppl. 1) 14–20, 1978.
 154. Johansson, B., and D. F. Bohr. Rhythmic activity in smooth muscle from small subcutaneous arteries. Am. J. Physiol. 210: 801–806, 1966.
 155. Johansson, B., and O. Jonsson. Cell volume as a factor influencing electrical and mechanical activity of vascular smooth muscle. Acta Physiol. Scand. 72: 456–468, 1968.
 156. Johansson, B., and O. Jonsson. Similarities between the vascular smooth muscle responses to sudden changes in external potassium, sodium and chloride ion concentrations. Acta Physiol. Scand. 73: 365–378, 1968.
 157. Johansson, B., and B. Ljung. Spread of excitation in the smooth muscle of the rat portal vein. Acta Physiol. Scand. 70: 312–322, 1967.
 158. Jonsson, O. Changes in the activity of isolated vascular smooth muscle in response to reduced osmolarity. Acta Physiol. Scand. 77: 191–200, 1969.
 159. Jonsson, O. Changes in the cell volume of isolated vascular smooth muscle in response to reduced osmolarity. Acta Physiol. Scand. 77: 201–211, 1969.
 160. Jonsson, O. Extracellular osmolarity and vascular smooth muscle activity. Acta Physiol. Scand. 81: (Suppl. 359) 1–48, 1970.
 161. Jonsson, O. Effects of variations in the extracellular osmolality on the ion permeability of vascular smooth muscle. Acta Physiol. Scand. 81: 405–421, 1971.
 162. Kalsner, S. Intrinsic prostaglandin release: a mediator of anoxia‐induced relaxation in an isolated coronary artery preparation. Blood Vessels 13: 155–166, 1976.
 163. Kalsner, S. The effect of hypoxia on prostaglandin output and on tone in isolated coronary arteries. Can. J. Physiol. Pharmacol. 55: 882–887, 1977.
 164. Katz, L. N., and E. Lindner. The action of excess Na, Ca, and K on the coronary vessels. Am. J. Physiol. 124: 155–160, 1938.
 165. Kjellmer, I. The effect of some physiological vasodilators on the vascular bed of skeletal muscles. Acta Physiol. Scand. 63: 94–105, 1965.
 166. Kjellmer, I. On the competition between metabolic vasodilation and neurogenic vasoconstriction in skeletal muscle. Acta Physiol. Scand. 63: 450–459, 1965.
 167. Kjellmer, I. The potassium ion as a vasodilator during muscular exercise. Acta Physiol. Scand. 63: 460–468, 1965.
 168. Knochel, J., and E. Schlein. On the mechanism of rhabdo‐myolysis in potassium depletion. J. Clin. Invest. 51: 1750–1758, 1972.
 169. Konold, P., G. Gebert, and K. Brecht. The antagonism of potassium and catecholamines on the vascular tone of isolated arterial segments. Experientia 24: 692, 1968.
 170. Konold, P., G. Gebert, and K. Brecht. The effect of potassium on the tone of isolated arteries. Pfluegers Arch. Ges. Physiol. 301: 285–291, 1968.
 171. Kontos, H. A., and R. R. Lower. Role of beta‐adrenergic receptors in the circulatory response to hypoxia. Am. J. Physiol. 217: 756–763, 1969.
 172. Kontos, H. A., D. W. Richardson, and J. L. Patterson, Jr. Blood flow and metabolism of forearm muscle in man at rest and during sustained contraction. Am. J. Physiol. 211: 869–876, 1966.
 173. Kontos, H. A., E. P. Wei, A. J. Roper, W. I. Rosenblum, R. M. Navari, and J. L. Patterson, Jr. Role of tissue hypoxia in local regulation of cerebral microcirculation. Am. J. Physiol. 234: H582–H591, 1978 or
 174. Am. J. Physiol.: Heart Circ. Physiol. 3: H582–H591, 1978.
 175. Kovalcik, V. The response of the isolated ductus arteriosis to oxygen and anoxia. J. Physiol. London 169: 185–197, 1963.
 176. Köver, G., T. Harza, W. Mályusz, and E. Szöcs. Protective effect of sucrose and mannitol against vasoconstriction induced by angiotensin II in the kidney. Acta Physiol. Acad. Sci. Hung. 33: 19–26, 1968.
 177. Kramer, K., F. Obal, and W. Quensel. Untersuchunger über den Muskelstoffwechseldes warmeblüters. III. Mittilung. Die saverstoffaufnahmedes Muskels während ryhthmischer Tatigkeit. Pfluegers Arch. Ges. Physiol. 241: 717–729, 1939.
 178. Krasney, J. A. Regional circulatory responses to arterial hypoxia in the anesthetized dog. Am. J. Physiol. 220: 699–704, 1971.
 179. Krishnamurtz, V. S. R., H. R. Adams, T. C. Smitherman, G. H. Templeton, and J. T. Willerson. Influence of mannitol on contractile responses of isolated perfused arteries. Am. J. Physiol. 232: H59–H66, 1977 or
 180. Am. J. Physiol.: Heart Circ. Physiol. 1: H59–H66, 1977.
 181. Kříž, N., Syková, E. Ujec, and L. Vyklický. Changes of extracellular potassium concentration induced by neuronal activity in the spinal cord of the cat. J. Physiol. London 238: 1–15, 1974.
 182. Kunze, D. L. Rate‐dependent changes in extracellular potassium in the rabbit atrium. Circulation Res. 41: 122–127, 1977.
 183. Kuriyama, H., K. Ohshima, and Y. Sakamato. The membrane properties of the smooth muscle of the guinea pig portal vein in isotonic and hypertonic solution. J. Physiol. London 217: 179–199, 1971.
 184. Kuschinsky, W., and M. Wahl. Interactions between perivascular norepinephrine and potassium or osmolarity on pial arteries of cats. Microvascular Res. 14: 173–180, 1977.
 185. Kuschinsky, W., M. Wahl, O. Bosse, and K. Thurau. The dependency of the pial arterial and arteriolar resistance on the perivascular H+ and K+ concentrations. European Neurol. 6: 92–95, 1971.
 186. Kuschinsky, W., M. Wahl, O. Bosse, and K. Thurau. Perivascular potassium and pH as determinants of local pial arterial diameter in cats: a microapplication study. Circulation Res. 31: 240–247, 1972.
 187. Lammerant, J., C. De Schryver, I. Becsei, M. Camphyn, and J. Mertensstrythagen. Coronary circulation response to hyperoxia after vagotomy and combined alpha and beta adrenergic receptors blockade in the anesthetized intact dog. Pfluegers Arch. European J. Physiol. 308: 185–196, 1969.
 188. Landis, E. M., and J. R. Pappenheimer. Exchange of substances through the capillary walls. In: Handbook of Physiology. Circulation, edited by W. F. Hamilton and P. Dow. Washington, D.C.: Am. Physiol. Soc., 1963, sect. 2, vol. II, chapt. 29, p. 961–1034.
 189. Laurell, H., and B. Pernow. Effect of exercise on plasma potassium of man. Acta Physiol. Scand. 66: 241–242, 1966.
 190. Leffler, C. W., T. L. Tyler, and S. Cassin. Effect of indo‐methacin on pulmonary vascular response to ventilation of fetal goats. Am. J. Physiol. 234: H346–H351, 1978 or
 191. Am. J. Physiol.: Heart Circ. Physiol. 3: H346–H351, 1978.
 192. Leniger‐Follert, E., and D. W. Lubbers. Behavior of microflow and local pO2 of the brain cortex during and after direct electrical stimulation: a contribution to the problem of metabolic regulation of microcirculation in the brain. Pfluegers Arch. European J. Physiol. 366: 39–44, 1976.
 193. Levine, S. E., D. N. Granger, R. A. Brace, and A. E. Taylor. Effect of hyperosmolality on vascular resistance and lymph flow in the cat ileum. Am. J. Physiol. 234: H14–H20, 1978 or
 194. Am. J. Physiol: Heart Circ. Physiol. 3: H14–H20, 1978.
 195. Limas, C. J., and J. N. Cohn. Stimulation of vascular smooth muscle sodium, potassium‐adenosinetriphosphatase by vasodilators. Circulation Res. 35: 601–607, 1974.
 196. Ljung, B., O. Isaksson, and B. Johansson. Levels of cyclic AMP and electrical events during inhibition of contractile activity in vascular smooth muscle. Acta Physiol. Scand. 94: 154–166, 1975.
 197. Lloyd, T. C.Jr. Hypoxic pulmonary vasoconstriction: role of perivascular tissue. J. Appl. Physiol. 25: 560–565, 1968.
 198. Lorenz, R. R., and P. M. Vanhoutte. Inhibition of adrenergic neurotransmission in isolated veins of the dog by potassium ions. J. Physiol. London 246: 479–500, 1975.
 199. Lundvall, J. Tissue hyperosmolality as a mediator of vasodilation and transcapillary fluid flux in exercising skeletal muscle. Acta Physiol. Scand. Suppl. 379: 1–142, 1972.
 200. Lundvall, J., and J. Halinberg. Role of tissue hyperosmolality in functional vasodilation in the submandibular gland. Acta Physiol. Scand. 92: 165–174, 1974.
 201. Lundvall, J., S. Mellander, and T. White. Hyperosmolarity and vasodilation in human skeletal muscle. Acta Physiol. Scand. 77: 224–233, 1969.
 202. Marshall, R. J., and J. T. Shepherd. Effect of injections of hypertonic solutions on blood flow through the femoral artery of the dog. Am. J. Physiol. 197: 951–954, 1959.
 203. Martini, J., and C. R. Honig. Direct measurement of intercapillary distance in beating rat heart in situ under various conditions of O2 supply. Microvascular Res. 1: 244–256, 1969.
 204. Maxwell, L. C., J. K. Barclay, D. E. Mohrman, and J. A. Faulkner. Physiological characteristics of skeletal muscles of dogs and cats. Am. J. Physiol. 233: C14–C18, 1977 or
 205. Am. J. Physiol.: Cell Physiol. 2: C14–C18, 1977.
 206. Maxwell, L. C., D. F. Bohr, and R. A. Murphy. Arterial actomyosis: effects of ionic strength on ATPase activity and solubility. Am. J. Physiol. 220: 1871–1874, 1971.
 207. McGilvery, R. W., and T. W. Murray. Calculated equilibria of phosphocreatine and adenosine phosphates during utilization of high energy phosphate by muscle. J. Biol. Chem. 249: 5845–5850, 1974.
 208. McGrath, M. A., and J. T. Shepherd. Hyper osmolarity: effects on nerves and smooth muscle of cutaneous veins. Am. J. Physiol. 231: 141–147, 1976.
 209. McKeever, W. P., H. Braun, S. Coder, and J. Croft. The local effects of potassium on different segments of the coronary vascular bed. Clin. Res. 8: 188, 1960.
 210. McKinley, M. J., J. S. McKenzie, and J. R. Blair‐West. Effects of maintained osmolarity changes on rat portal vein spontaneous contractions. Am. J. Physiol. 226: 718–723, 1974.
 211. McNeill, T. A. Venous oxygen saturation and blood flow during reactive hyperemia in the human forearm. J. Physiol. London 134: 195–201, 1956.
 212. Mellander, S., B. Johansson, S. Gray, O. Jonsson, J. Lundvall, and B. Ljung. The effects of hyper osmolarity on intact and isolated vascular smooth muscle: possible role in exercise hyperemia. Angiologica 4: 310–322, 1967.
 213. Mellander, S., and J. Lundvall. Role of tissue hyperosmolality in exercise hyperemia. Circulation Res. 28: (Suppl. I) 139–145, 1971.
 214. Mentzer, R. M.Jr., R. Rubio, and R. M. Berne. Release of adenosine by hypoxic canine lung tissue and its possible role in the pulmonary circulation. Am. J. Physiol. 229: 1625–1631, 1975.
 215. Meyer, J. S., T. Kanda, Y. Shinohara, and Y. Fukurchi. Changes in cerebrospinal fluid sodium and potassium concentration during seizure activity. Neurology 20: 1179–1184, 1970.
 216. Meyer, J. S., T. Kanda, Y. Shinohara, and Y. Fukurchi. Effects of anoxia on cerebrospinal fluid sodium and potassium concentrations. Neurology 21: 889–895, 1971.
 217. Middleman, S. Transport Phenomena in the Cardiovascular System. New York: Wiley, 1972, p. 135–138.
 218. Mohrman, D. E., J. R. Cant, and H. V. Sparks. Time course of vascular resistance and venous oxygen changes following brief tetanus of dog skeletal muscle. Circulation Res. 33: 323–336, 1973.
 219. Mohrman, D. E., and E. O. Feigl. Completion between sympathetic vasoconstriction and metabolic vasodilation in the canine coronary circulation. Circulation Res. 42: 79–86, 1978.
 220. Mohrman, D. E., and H. V. Sparks. Resistance and venous oxygen dynamics during sinusoidal exercise of dog skeletal muscle. Circulation Res. 33: 337–345, 1973.
 221. Mohrman, D. E., and H. V. Sparks. Myogenic hyperemia following brief tetanus of canine skeletal muscle. Am. J. Physiol. 227: 531–535, 1974.
 222. Mohrman, D. E., and H. V. Sparks. Role of potassium ions in the vascular response to a brief tetanus. Circulation Res. 35: 384–390, 1974.
 223. Morganroth, M. L., D. E. Mohrman, and H. V. Sparks. Prolonged vasodilation following fatiguing exercise of dog skeletal muscle. Am. J. Physiol. 229: 38–43, 1975.
 224. Müller‐Ruchholtz, E. R., and W. A. Neill. The mechanism of coronary hyperemia induced by increased cardiac work. Pfluegers Arch. European J. Physiol. 361: 197–199, 1976.
 225. Murray, P. A., and H. V. Sparks. The role of K+ in the control of coronary vascular resistance. Physiologist 19: 307, 1976.
 226. Murray, P. A., and H. V. Sparks. The mechanism of K+‐induced vasodilation of the coronary vascular bed of the dog. Circulation Res. 42: 35–42, 1978.
 227. Nair, X., and D. C. Dyer. Effect of metabolic inhibitors and oxygen on responses of human umbilical arteries. Am. J. Physiol. 225: 1118–1122, 1973.
 228. Namm, D. H., and J. L. Zucker. Biochemical alterations caused by hypoxia in the isolated rabbit aorta. Circulation Res. 32: 464–470, 1973.
 229. Needleman, P., and D. J. Blehm. Effect of epinephrine and potassium chloride on contraction and energy intermediate in rabbit thoracic aorta strips. Life Sci. 9: 1181–1189, 1970.
 230. Noel, S., and S. Cassin. Maturation of contractile response of ductus arteriosus to oxygen and drugs. Am. J. Physiol. 231: 240–243, 1976.
 231. Norman, J. N., J. R. Shearer, A. J. Napper, I. M. Robertson, and G. Smith. Action of oxygen on the renal circulation. Am. J. Physiol. 227: 740–744, 1974.
 232. Norton, J. M., and R. Detar. Potassium and isolated coronary vascular smooth muscle. Am. J. Physiol. 222: 474–479, 1972.
 233. Olsson, R. A. Brief reviews: myocardial reactive hyperemia. Circulation Res. 37: 263–270, 1975.
 234. Olsson, R. A., and D. E. Gregg. Metabolic responses during myocardial reactive hyperemia in the unanesthetized dog. Am. J. Physiol. 208: 231–236, 1965.
 235. Overbeck, H. W., R. S. Derifield, M. B. Pamnani, and T. Sözen. Attenuated vasodilator responses to K+ in essential hypertensive men. J. Clin. Invest. 53: 678–686, 1974.
 236. Overbeck, H. W., and G. J. Grega. Response of the limb vascular bed in man to intrabrachial arterial infusions of hypertonic dextrose or hypotonic sodium chloride solutions. Circulation Res. 26: 717–731, 1970.
 237. Overbeck, H. W., J. I. Molnar, and F. J. Haddy. Resistance to blood flow through the vascular bed of the dog forelimb. Am. J. Cardiol. 8: 533–541, 1961.
 238. Paul, R. J. Oxygen tension sensors in vascular smooth muscle. In: Tissue Hypoxia and Ischemia, edited by M. Reivich, R. F. Coburn, S. Lahiri, and B. Chance. New York: Plenum, 1977, p. 117–121.
 239. Peterson, J. W., and R. J. Paul. Aerobic glycolysis in vascular smooth muscle: relation to isometric tension. Biochim. Biophys. Acta 357: 167–176, 1974.
 240. Pittman, R. N., and B. R. Duling. Oxygen sensitivity of vascular smooth muscle. Microvascular Res. 6: 202–211, 1973.
 241. Pohost, G. M., J. B. Newell, N. P. Hamlin, and W. J. Powell, Jr. Observations on autoregulation in skeletal muscle: the effects of arterial hypoxia. Cardiovascular Res. 10: 405–412, 1976.
 242. Ponte, J., and M. J. Purves. The role of the carotid body chemoreceptors and carotid sinus baroreceptors in the control of cerebral blood vessels. J. Physiol. London 237: 315–340, 1974.
 243. Prewitt, R. L., and P. C. Johnson. The effect of oxygen on arteriolar red cell velocity and capillary density in the rat cremaster muscle. Microvascular Res. 12: 59–70, 1976.
 244. Radawski, D. P., W. Hoppe, and F. J. Haddy. Role of vasoactive substances in active hyperemia in skeletal muscle. Proc. Soc. Exptl. Biol. Med. 148: 270–276, 1975.
 245. Raizner, A. E., J. C. Costin, R. P. Croke, J. B. Bishop, T. V. Inglesby, and N. S. Skinner, Jr. Reflex, systemic, and local hemodynamic alterations with experimental hyperosmolality. Am. J. Physiol. 224: 1327–1333, 1973.
 246. Reuter, H., M. P. Blaustein, and G. Hoesler. Na‐Ca exchange and tension development in arterial smooth muscle. Phil. Trans. Roy. Soc. London Ser. B 265: 87–94, 1973.
 247. Ross, J. M., H. M. Fairchild, J. Weldy, and A. C. Guyton. Autoregulation of flow by oxygen lack. Am. J. Physiol. 202: 21–24, 1962.
 248. Rothlin, E. Experimentelle studien über die Eigenschaften überlebender Gefäsze unter Anwendung der chemischen Reiz‐methode. Biochem. Z. 111: 219–256, 1920.
 249. Rubio, R., and R. M. Berne. Myocardium. In: Peripheral Circulation, edited by P. C. Johnson. New York: Wiley, 1978, p. 231–254.
 250. Rubio, R., V. T. Wiedmeir, and R. M. Berne. Relationship between coronary flow and adenosine production and release. J. Mol. Cellular Cardiol. 6: 561–566, 1974.
 251. Said, S. I., and N. Hara. Prostaglandins and the pulmonary vasoconstrictor response to alveolar hypoxia. Science 189: 900, 1975.
 252. Said, S. I., T. Yoshida, S. Kitamura, and C. Vreim. Pulmonary alveolar hypoxia: release of prostaglandins and other humoral mediators. Science 185: 1181–1183, 1974.
 253. Saltzman, H. A., L. Hart, H. O. Sieker, and E. J. Duffy. Retinal vascular response to hyperbaric oxygenation. J. Am. Med. Assoc. 191: 290–292, 1965.
 254. Sarnoff, S. J., J. P. Gilmore, R. H. McDonald, Jr., W. M. Daggett, M. L. Weisfeldt, and P. B. Mansfield. Relationship between myocardial K+ balance, O2 consumption, and contractility. Am. J. Physiol. 211: 361–375, 1966.
 255. Schnaar, R. L., and H. V. Sparks. Response of large and small coronary arteries to nitroglycerin, NaNO2, and adenosine. Am. J. Physiol. 223: 223–228, 1972.
 256. Schubert, R. W., W. J. Whalen, and P. Nair. Myocardial Po2 distribution: relationship to coronary autoregulation. Am. J. Physiol. 234: H361–H370, 1978 or
 257. Am. J. Physiol.: Heart Circ. Physiol. 3: H361–H370, 1978.
 258. Schuchhardt, S., and L. Osse. Static and dynamic behavior of local oxygen pressure in the myocardium. Bibliotheca Anat. 11: 164–168, 1973.
 259. Scott, J. B., and D. Radawski. Role of hyper osmolarity in the genesis of active and reactive hyperemia. Circulation Res. 28: (Suppl. 1) 26–32, 1971.
 260. Scott, J. B., M. Rudko, D. Radawski, and F. J. Haddy. Role of osmolarity, K+, H+, Mg++ and O2 in local blood flow regulation. Am. J. Physiol. 218: 338–345, 1970.
 261. Sheehan, R. M., and E. M. Renkin. Capillary interstitial and cell membrane barriers to blood‐tissue transport of potassium and rubidium in mammalian skeletal muscle. Circulation Res. 30: 588–607, 1972.
 262. Shepherd, A. P. Intestinal O2 consumption and 86Rb extraction during arterial hypoxia. Am. J. Physiol. 234: E248–E251, 1978 or
 263. Am. J. Physiol.: Endocrinol. Metab. Gastrointest. Physiol. 3: E248–E251, 1978.
 264. Shepherd, A. P., H. J. Granger, E. E. Smith, and A. C. Guyton. Local control of tissue oxygen delivery and its contribution to the regulation of cardiac output. Am. J. Physiol. 225: 747–755, 1973.
 265. Shibata, S., and A. H. Briggs. Mechanical activity of vascular smooth muscle under anoxia. Am. J. Physiol. 212: 981–984, 1967.
 266. Silove, E. D., and A. J. Simcha. Histamine‐induced pulmonary vasodilatation in the calf: relationship to hypoxia. J. Appl. Physiol. 35: 830–836, 1973.
 267. Skinner, N. S. Skeletal‐muscle blood flow: metabolic determinants. In: Peripheral Circulations, edited by R. Zelis. New York: Grune & Stratton, 1975, p. 57–78.
 268. Skinner, N. S.Jr., and J. C. Costin. Role of O2 and K+ in abolition of sympathetic vasoconstriction in dog skeletal muscle. Am. J. Physiol. 217: 438–444, 1969.
 269. Skinner, N. S.Jr., and J. C. Costin. Interactions of vasoactive substances in exercise hyperemia: O2, K+, and osmolality. Am. J. Physiol. 219: 1386–1392, 1970.
 270. Skinner, S. N., and J. C. Costin. Interactions between oxygen, potassium, and osmolarity in regulation of skeletal muscle blood flow. Circulation Res. 28: (Suppl. 1) 73–85, 1971.
 271. Smith, D. J., and J. R. Vane. Effects of oxygen tension on vascular and other smooth muscle. J. Physiol. London 186: 284–294, 1966.
 272. Smith, R. H., E. J. Guilbeau, and D. D. Reneau. The oxygen tension field within a discrete volume of cerebral cortex. Microvascular Res. 13: 233–240, 1977.
 273. Somlyo, A. P., and A. V. Somlyo. Vascular smooth muscle. I. Normal structure, pathology, biochemistry, and biophysics. Pharmacol. Rev. 20: 197–272, 1968.
 274. Souhrada, J. F., and D. W. Dickey. Effect of substrate on hypoxic response of pulmonary artery. J. Appl. Physiol. 40: 533–538, 1976.
 275. Sparks, H. V. Skin and muscle. In: Peripheral Circulation, edited by P. C. Johnson. New York: Wiley, 1978, p. 193–230.
 276. Stainsby, W. N., and J. K. Barclay. Effect of infusions of osmotically active substances on muscle blood flow and systemic blood pressure. Circulation Res. 28: (Suppl. 1) 33–38, 1971.
 277. Stainsby, W. N., and M. J. Fregley. Effect of plasma osmolality on resistance to blood flow through skeletal muscle. Proc. Soc. Exptl. Biol. Med. 128: 284–287, 1968.
 278. Starling, M. F., and R. B. Elliott. The effects of prostaglandins, prostaglandin inhibitors, and oxygen on the closure of the ductus arteriosus, pulmonary arteries and umbilical vessels in vitro. Prostaglandins 8: 187–203, 1974.
 279. Staub, N. C. The sensing of oxygen tension on the pulmonary circulation. In: Tissue Hypoxia and Ischemia, edited by M. Reivich, R. F. Coburn, S. Lahiri, and B. Chance. New York: Plenum, 1977, p. 151–161.
 280. Stowe, D. F., T. L. Owen, D. K. Anderson, F. J. Haddy, and J. B. Scott. Interaction of O2 and CO2 in sustained exercise hyperemia of canine skeletal muscle. Am. J. Physiol. 229: 28–33, 1975.
 281. Sugashita, Y., M. Kakihara, and S. Murao. Decreased reactive hyperemia after coronary perfusion with monoxygenated solution. Am. J. Physiol. 234: H625–H628, 1978 or
 282. Am. J. Physiol.: Heart Circ. Physiol. 3: H625–H628, 1978.
 283. Susmano, A., and R. A. Carleton. Prevention of hypoxic pulmonary hypertension by chlorpheniramine. J. Appl. Physiol. 31: 531–535, 1971.
 284. Sybers, R. G., H. D. Sybers, P. R. Helmer, and Q. R. Murphy. Myocardial potassium balance during cardioaccelerator nerve and atrial stimulation. Am. J. Physiol. 209: 699–701, 1965.
 285. Szidon, J. P., and J. F. Flint. Significance of sympathetic innervation of pulmonary vessels in response to acute hypoxia. J. Appl. Physiol. 43: 65–71, 1977.
 286. Tancredi, R. G., T. Yipintsoi, and J. B. Bassingthwaighte. Capillary and cell wall permeability to potassium in isolated dog hearts. Am. J. Physiol. 229: 537–544, 1975.
 287. Tibes, U., B. Hemmer, D. Böning, and U. Schweigart. Relationships of femoral venous [K+], [H+], Po2, osmolarity, and [orthophosphate] with heart rate, ventilation, and leg blood flow during bicycle exercise in athletes and non‐athletes. European J. Appl. Physiol. Occupational Therap. 35: 201–214, 1976.
 288. Toda, N. Responsiveness to potassium and calcium ions of isolated cerebral arteries. Am. J. Physiol. 227: 1206–1211, 1974.
 289. Toda, N. Potassium‐induced relaxation in isolated cerebral arteries contracted with prostaglandin F2a. Pfluegers Arch. European J. Physiol. 364: 235–242, 1976.
 290. Toda, N. Mechanical responses of isolated dog cerebral arteries to reduction of external K, Na, and Cl. Am. J. Physiol. 234: H404–H411, 1978 or
 291. Am. J. Physiol.: Heart Circ. Physiol. 3: H404–H411, 1978.
 292. Tominaga, S., T. Suzuki, and T. Nakamura. Evaluation of the roles of potassium, inorganic phosphate, osmolarity, pH, Pco2, Po2, and adenosine or AMP in exercise and reactive hyperemia in canine hindlimb muscles. Tohoku J. Exptl. Med. 109: 347–363, 1973.
 293. Tuma, R. F., L. Lindbom, and K.‐E. Arfors. Dependence of reactive hyperemia in skeletal muscle on oxygen tension. Am. J. Physiol. 233: H289–H294, 1977 or
 294. Am. J. Physiol.: Heart Circ. Physiol. 2: H289–H294, 1977.
 295. Tyler, T., R. Wallis, C. Leffler, and S. Cassin. The effects of indomethacin on the pulmonary vascular response to hypoxia in the premature and mature newborn goat. Proc. Soc. Exptl. Biol. Med. 150: 695–698, 1975.
 296. Uvelius, B., and B. Johansson. Relation between extracellular potassium ion concentration and contracture force after abolition of spike discharge in isolated rat portal vein. Blood Vessels 11: 120–127, 1974.
 297. Vaage, J., L. Bjertnaes, and A. Hauge. The pulmonary vasoconstrictor response to hypoxia: effects of inhibitors of prostaglandin biosynthesis. Acta Physiol. Scand. 95: 95–101, 1975.
 298. Vaage, J., and A. Hauge. Prostaglandins and the pulmonary vasoconstrictor response to alveolar hypoxia. Science 189: 899–900, 1975.
 299. Van Harn, G. L., R. Rubio, and R. M. Berne. Formation of adenosine nucleotide derivatives in isolated hog carotid artery strips. Am. J. Physiol. 233: H299–H304, 1977 or
 300. Am. J. Physiol.: Heart Circ. Physiol. 2: H299–H304, 1977.
 301. Vanhoutte, P. M. Effects of anoxia and glucose depletion on isolated veins of the dog. Am. J. Physiol. 230: 1261–1268, 1976.
 302. Vanhoutte, P. M., and R. R. Lorenz. Inhibition of norepinephrine uptake by potassium ions in vascular smooth muscle. Arch. Intern. Pharmacodyn. Therap. 208: 377, 1974.
 303. Van Liew, H. D., and B. Rodgers. Variability of partial pressures of CO2 and O2 in resting skeletal muscle. Microvascular Res. 10: 127–137, 1975.
 304. Verhaeghe, R. H., R. R. Lorenz, M. A. McGrath, J. T. Shepherd, and P. M. Vanhoutte. Metabolic modulation of neurotransmitter release—adenosine, adenine nucleotides, potassium, hyperosmolarity, and hydrogen ion. Federation Proc. 37: 208–211, 1978.
 305. Wahl, M., W. Kuschinsky, O. Bosse, and K. Thurau. Dependency of pial arterial and arteriolar diameter on perivascular osmolarity in the cat. A microapplication study. Circulation Res. 32: 162–169, 1973.
 306. Wahlstrom, B. The effect of changes in the ionic environment on venous smooth muscle distribution of sodium and potassium. Acta Physiol. Scand. 82: 382–392, 1971.
 307. Walker, J. R., and A. Guyton. Influence of blood oxygen saturation on pressure‐flow curve of dog hindleg. Am. J. Physiol. 212: 506–509, 1967.
 308. Weir, E. K., I. F. McMurtry, A. Tucker, J. T. Reeves, and R. F. Grover. Prostaglandin synthetase inhibitors do not decrease hypoxic pulmonary vasoconstriction. J. Appl. Physiol. 41: 714–718, 1976.
 309. Whalen, W. J., D. Buerk, and C. A. Thuning. Blood flow‐limited oxygen consumption in resting cat skeletal muscle. Am. J. Physiol. 224: 763–768, 1973.
 310. Whalen, W. J., and P. Nair. Intracellular pO2 and its regulation in resting skeletal muscle of the guinea pig. Circulation Res. 21: 251–262, 1967.
 311. Wiberg, T., J. Vaage, L. Bjertnaes, A. Hauge, and K. M. Gautrick. Prostaglandin in blood and lung tissue during alveolar hypoxia. Acta Physiol. Scand. 102: 181–190, 1978.
 312. Wilson, D. F., M. Erecînska, C. Drown, and I. A. Silver. Effect of oxygen tension on cellular energetics. Am. J. Physiol. 233: C135–C140, 1977 or
 313. Am. J. Physiol.: Cell Physiol. 2: C135–C140, 1977.
 314. Yam, J., and R. J. Roberts. Modification of alveolar hyperoxia induced pulmonary vasodilation by indomethacin. Prostaglandins 11: 679–689, 1976.
 315. Yonce, L. R., and W. F. Hamilton. Oxygen consumption in skeletal muscle during reactive hyperemia. Am. J. Physiol. 197: 190–192, 1959.
 316. Young, S. H., and H. L. Stone. Effect of a reduction in arterial oxygen content (carbon monoxide) on coronary flow. Aviat. Space Environ. Med. 47: 142–146, 1976.
 317. Ziegler, W. H., and C. A. Goresky. Transcapillary exchange in the working left ventricle of the dog. Circulation Res. 29: 181–207, 1971.
 318. Ziegler, W. H., and C. A. Goresky. Kinetics of rubidium uptake in the working dog heart. Circulation Res. 29: 208–220, 1971.

Contact Editor

Submit a note to the editor about this article by filling in the form below.

* Required Field

How to Cite

Harvey V. Sparks. Effect of Local Metabolic Factors on Vascular Smooth Muscle. Compr Physiol 2011, Supplement 7: Handbook of Physiology, The Cardiovascular System, Vascular Smooth Muscle: 475-513. First published in print 1980. doi: 10.1002/cphy.cp020217