Comprehensive Physiology Wiley Online Library

The Myogenic Response

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Historical Background
2 Response to Quick Stretch
2.1 Nonvascular Smooth Muscle
2.2 Vascular Smooth Muscle
2.3 Response of Blood Vessels in situ
3 Response to Sustained Force or Pressure
3.1 Nonvascular Smooth Muscle
3.2 Isolated Vascular Smooth Muscle Preparations
3.3 Pressure‐Flow and Microcirculatory Studies
4 The Myogenic Concept
4.1 Transmission of Myogenic Activity
4.2 Behavior of a Myogenically Controlled Network
5 Homeostatic Significance of Myogenic Mechanism
Figure 1. Figure 1.

Sir William Maddock Bayliss (1860–1924).

Photograph courtesy Mr. C. A. N. Evans, Department of Physiology, University College, London
Figure 2. Figure 2.

Volume changes (upper trace) and arterial pressure recording (lower trace) from hindlimb of dog with occlusion of the supply artery for 8 s and then for 20 s.

From Bayliss
Figure 3. Figure 3.

Contraction of isolated carotid artery with pressure elevation.

From Wachholder
Figure 4. Figure 4.

Effect of alteration in perfusion pressure on blood flow in perfused hindquarters of cat. Blood flow increase is transient when pressure is elevated from 150 to 200 mmHg (panel A) and from 130 to 180 mmHg (panel C).

From Folkow
Figure 5. Figure 5.

Reactions of various types of smooth muscle to quick stretch. Upward deflection indicates increase in tension. Arrow indicates instant that quick stretch is applied. Panel g: muscle is held in elongated state for several seconds (upper trace) or subjected to slow stretch (lower trace).

From Burnstock and Prosser
Figure 6. Figure 6.

Effect of stretch of varying rate and amplitude on contractile response of human umbilical artery strips. A: effect of varying stretch rate; B: effect of varying amplitude; C: effect of initial tension on response.

From Sparks , by permission of the American Heart Association, Inc
Figure 7. Figure 7.

Effect of stretch on mechanical and electrical activity of guinea pig portal vein. Shown are reactions to stretch rate of 1 mm/min (upper panel) and 4 mm/min (lower panel). Note increased mechanical and electrical activity with dynamic stretch. Both parameters are also somewhat elevated during maintained stretch.

From Johansson and Mellander , by permission of the American Heart Association, Inc
Figure 8. Figure 8.

Effect of sudden pressure elevations in vascular resistance and flow in isolated kidney.

From Waugh , by permission of the American Heart Association, Inc
Figure 9. Figure 9.

Arteriolar response after 2‐min arterial occlusion in cat sartorius muscle. Note period of strong arteriolar constriction and complete flow stoppage after pressure elevation. Dilatation during arterial occlusion is also apparent.

Courtesy of Sharon Sullivan, Dept. of Physiology, Univ. of Arizona
Figure 10. Figure 10.

Response of gracilis muscle vasculature to pulsatile perfusion. Left panels show decrease in flow with pulsatile pressure. Right panels illustrate absence of effect in passive preparation treated with papaverine. Perfusion pressure in mmHg. Venous outflow in ml/min.

From LaLone
Figure 11. Figure 11.

Upper graph, relation between membrane potential and length of taenia coli; lower graph, relation of membrane potential to applied tension.

From Bülbring
Figure 12. Figure 12.

Patterns of autoregulation in various vascular beds. Solid circles, steady state values; open circles, transient values after sudden pressure change from control level of 100 mmHg.

Kidney data from Rothe et al. , brain flow data from Rapela and Green , coronary flow data from Cross , and skeletal muscle flow data from Jones and Berne
Figure 13. Figure 13.

Patterns of flow (red cell velocity) in capillary of cat mesentery during stepwise reduction in perfusion pressure. Reduction of mean pressure from 100 to 80 mmHg caused loss of periodic flow and increase in mean red cell velocity. Subsequent pressure reductions caused decline in red cell velocity. Note resumption of periodic flow after period of elevated flow (reactive hyperemia) when pressure was restored.

From Johnson and Wayland
Figure 14. Figure 14.

Effect of arterial pressure reduction from 90 to 60 mmHg in a vessel with complete downstream micro‐occlusion. Repeated pressure reductions consistently produced vasodilatation.

From Johnson and Intaglietta
Figure 15. Figure 15.

Effect of venous pressure elevation on vascular resistance.

Data for intestine from Johnson , for colon from Hanson and Johnson , and for liver from Hanson and Johnson
Figure 16. Figure 16.

Arterial pressure was reduced to 60 mmHg after 60‐s control period. This reduction caused a momentary drop in flow then a return to near normal levels with loss of vasomotion. Subsequent elevation of venous pressure from 0 to 6 mmHg caused decline in flow and return of vasomotion.

From Johnson and Wayland
Figure 17. Figure 17.

Effect of venous pressure elevation on diameter of arteriole (A), metarteriole (M), precapillary sphincter (pC), and venule (V). Diameters measured with image‐splitting device. Measurements repeated in same sequence during elevated venous pressure. Diameter change in arteriole was exceptionally large. 2 ri % refers to percentage change in diameter.

From Baez et al.
Figure 18. Figure 18.

Plot of pressure profile in peripheral circulation, showing effect of increase of 10 mmHg in arterial pressure (left panel) or similar increase in venous pressure (right panel). Upper graph in each panel shows percentage increase in pressure as a function of position in the vascular network. Po, original pressure; Pi, increased pressure; ΔP, pressure change.

From Johnson
Figure 19. Figure 19.

Plot of arteriolar internal diameter with step change in static intravascular pressure. Studies done while blood flow was arrested in isolated cat mesenteric preparation and arterial and venous pressure were elevated simultaneously.

From Johnson and Intaglietta
Figure 20. Figure 20.

Effect of downstream occlusion on pressure and diameter in bat wing venule. Note increase in contraction frequency that accompanies increase in pressure (A) and diameter (B).

From Wiederhielm
Figure 21. Figure 21.

Plot of lymphatic contraction frequency as function of transmural pressure and wall tension. Tension calculated from Laplace equation.

From Hargens and Zweifach
Figure 22. Figure 22.

Two models of myogenic mechanism. Parallel model (left panel) consists of excitable cell membrane (EM) in parallel with contractile machinery (CM), shown here composed of viscous and elastic elements. Series model (right panel) consists of excitable cell membrane in series with contractile machinery. In lower section of each panel, response of the model to applied force is shown for situations of low gain (curve a), and high gain (curve b).

Figure 23. Figure 23.

Postulated mechanism for myogenic response leading to decrease in mean vessel diameter with increased intravascular pressure, based upon parallel arrangement of excitable membrane and contractile element.

From Folkow , by permission of the American Heart Association, Inc
Figure 24. Figure 24.

Change in arteriolar diameter and arteriolar volume flow with stepwise reduction of arterial pressure. Upper panel shows response of vessel that exhibited vasomotion. Lower panel shows response of vessel that did not show periodic contraction. Note increase in arteriolar volume flow with pressure reduction in both examples. Data from isolated cat sartorius muscle.

From LaLone and Johnson, unpublished data
Figure 25. Figure 25.

Schematic diagram showing arrangement of contractile elements within smooth muscle cell of Bufo marinus stomach.

From Fay et al.
Figure 26. Figure 26.

Diagram of series model of myogenic mechanism as applied to arteriole.

From Johnson
Figure 27. Figure 27.

Estimated wall tension in mesenteric arterioles with stepwise reduction in arterial pressure. Data points are from two series of experiments in which initial pressure was 100 mmHg and 80 mmHg, respectively. Dashed lines show tension change that would be expected if arteriolar diameter remained constant as arterial pressure was lowered.

From Johnson and Intaglietta
Figure 28. Figure 28.

Postulated change in arteriolar radius (upper panel) and arteriolar volume flow (lower panel) with a series model myogenic tension receptor. Gains indicated are closed‐loop gains of myogenic model.

From Johnson and Intaglietta
Figure 29. Figure 29.

Diagram illustrating behavior of series‐coupled myogenic effectors. Upper panel shows consecutive vascular segments. Lower panel illustrates pressure gradient in control state and at reduced pressure. 1, control; 2, after 20% arterial pressure reduction; 3, after 40% arterial pressure reduction. For purposes of illustration, the pressure gradient is taken to be more nearly linear than is the case in the arteriolar network.

From LaLone and Johnson, unpublished data


Figure 1.

Sir William Maddock Bayliss (1860–1924).

Photograph courtesy Mr. C. A. N. Evans, Department of Physiology, University College, London


Figure 2.

Volume changes (upper trace) and arterial pressure recording (lower trace) from hindlimb of dog with occlusion of the supply artery for 8 s and then for 20 s.

From Bayliss


Figure 3.

Contraction of isolated carotid artery with pressure elevation.

From Wachholder


Figure 4.

Effect of alteration in perfusion pressure on blood flow in perfused hindquarters of cat. Blood flow increase is transient when pressure is elevated from 150 to 200 mmHg (panel A) and from 130 to 180 mmHg (panel C).

From Folkow


Figure 5.

Reactions of various types of smooth muscle to quick stretch. Upward deflection indicates increase in tension. Arrow indicates instant that quick stretch is applied. Panel g: muscle is held in elongated state for several seconds (upper trace) or subjected to slow stretch (lower trace).

From Burnstock and Prosser


Figure 6.

Effect of stretch of varying rate and amplitude on contractile response of human umbilical artery strips. A: effect of varying stretch rate; B: effect of varying amplitude; C: effect of initial tension on response.

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


Figure 7.

Effect of stretch on mechanical and electrical activity of guinea pig portal vein. Shown are reactions to stretch rate of 1 mm/min (upper panel) and 4 mm/min (lower panel). Note increased mechanical and electrical activity with dynamic stretch. Both parameters are also somewhat elevated during maintained stretch.

From Johansson and Mellander , by permission of the American Heart Association, Inc


Figure 8.

Effect of sudden pressure elevations in vascular resistance and flow in isolated kidney.

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


Figure 9.

Arteriolar response after 2‐min arterial occlusion in cat sartorius muscle. Note period of strong arteriolar constriction and complete flow stoppage after pressure elevation. Dilatation during arterial occlusion is also apparent.

Courtesy of Sharon Sullivan, Dept. of Physiology, Univ. of Arizona


Figure 10.

Response of gracilis muscle vasculature to pulsatile perfusion. Left panels show decrease in flow with pulsatile pressure. Right panels illustrate absence of effect in passive preparation treated with papaverine. Perfusion pressure in mmHg. Venous outflow in ml/min.

From LaLone


Figure 11.

Upper graph, relation between membrane potential and length of taenia coli; lower graph, relation of membrane potential to applied tension.

From Bülbring


Figure 12.

Patterns of autoregulation in various vascular beds. Solid circles, steady state values; open circles, transient values after sudden pressure change from control level of 100 mmHg.

Kidney data from Rothe et al. , brain flow data from Rapela and Green , coronary flow data from Cross , and skeletal muscle flow data from Jones and Berne


Figure 13.

Patterns of flow (red cell velocity) in capillary of cat mesentery during stepwise reduction in perfusion pressure. Reduction of mean pressure from 100 to 80 mmHg caused loss of periodic flow and increase in mean red cell velocity. Subsequent pressure reductions caused decline in red cell velocity. Note resumption of periodic flow after period of elevated flow (reactive hyperemia) when pressure was restored.

From Johnson and Wayland


Figure 14.

Effect of arterial pressure reduction from 90 to 60 mmHg in a vessel with complete downstream micro‐occlusion. Repeated pressure reductions consistently produced vasodilatation.

From Johnson and Intaglietta


Figure 15.

Effect of venous pressure elevation on vascular resistance.

Data for intestine from Johnson , for colon from Hanson and Johnson , and for liver from Hanson and Johnson


Figure 16.

Arterial pressure was reduced to 60 mmHg after 60‐s control period. This reduction caused a momentary drop in flow then a return to near normal levels with loss of vasomotion. Subsequent elevation of venous pressure from 0 to 6 mmHg caused decline in flow and return of vasomotion.

From Johnson and Wayland


Figure 17.

Effect of venous pressure elevation on diameter of arteriole (A), metarteriole (M), precapillary sphincter (pC), and venule (V). Diameters measured with image‐splitting device. Measurements repeated in same sequence during elevated venous pressure. Diameter change in arteriole was exceptionally large. 2 ri % refers to percentage change in diameter.

From Baez et al.


Figure 18.

Plot of pressure profile in peripheral circulation, showing effect of increase of 10 mmHg in arterial pressure (left panel) or similar increase in venous pressure (right panel). Upper graph in each panel shows percentage increase in pressure as a function of position in the vascular network. Po, original pressure; Pi, increased pressure; ΔP, pressure change.

From Johnson


Figure 19.

Plot of arteriolar internal diameter with step change in static intravascular pressure. Studies done while blood flow was arrested in isolated cat mesenteric preparation and arterial and venous pressure were elevated simultaneously.

From Johnson and Intaglietta


Figure 20.

Effect of downstream occlusion on pressure and diameter in bat wing venule. Note increase in contraction frequency that accompanies increase in pressure (A) and diameter (B).

From Wiederhielm


Figure 21.

Plot of lymphatic contraction frequency as function of transmural pressure and wall tension. Tension calculated from Laplace equation.

From Hargens and Zweifach


Figure 22.

Two models of myogenic mechanism. Parallel model (left panel) consists of excitable cell membrane (EM) in parallel with contractile machinery (CM), shown here composed of viscous and elastic elements. Series model (right panel) consists of excitable cell membrane in series with contractile machinery. In lower section of each panel, response of the model to applied force is shown for situations of low gain (curve a), and high gain (curve b).



Figure 23.

Postulated mechanism for myogenic response leading to decrease in mean vessel diameter with increased intravascular pressure, based upon parallel arrangement of excitable membrane and contractile element.

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


Figure 24.

Change in arteriolar diameter and arteriolar volume flow with stepwise reduction of arterial pressure. Upper panel shows response of vessel that exhibited vasomotion. Lower panel shows response of vessel that did not show periodic contraction. Note increase in arteriolar volume flow with pressure reduction in both examples. Data from isolated cat sartorius muscle.

From LaLone and Johnson, unpublished data


Figure 25.

Schematic diagram showing arrangement of contractile elements within smooth muscle cell of Bufo marinus stomach.

From Fay et al.


Figure 26.

Diagram of series model of myogenic mechanism as applied to arteriole.

From Johnson


Figure 27.

Estimated wall tension in mesenteric arterioles with stepwise reduction in arterial pressure. Data points are from two series of experiments in which initial pressure was 100 mmHg and 80 mmHg, respectively. Dashed lines show tension change that would be expected if arteriolar diameter remained constant as arterial pressure was lowered.

From Johnson and Intaglietta


Figure 28.

Postulated change in arteriolar radius (upper panel) and arteriolar volume flow (lower panel) with a series model myogenic tension receptor. Gains indicated are closed‐loop gains of myogenic model.

From Johnson and Intaglietta


Figure 29.

Diagram illustrating behavior of series‐coupled myogenic effectors. Upper panel shows consecutive vascular segments. Lower panel illustrates pressure gradient in control state and at reduced pressure. 1, control; 2, after 20% arterial pressure reduction; 3, after 40% arterial pressure reduction. For purposes of illustration, the pressure gradient is taken to be more nearly linear than is the case in the arteriolar network.

From LaLone and Johnson, unpublished data
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Paul C. Johnson. The Myogenic Response. Compr Physiol 2011, Supplement 7: Handbook of Physiology, The Cardiovascular System, Vascular Smooth Muscle: 409-442. First published in print 1980. doi: 10.1002/cphy.cp020215