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Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis

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Abstract

The sections in this article are:

1 Historical Background
1.1 Renin
1.2 Aldosterone
1.3 A Coordinated Renal‐Adrenal Hormonal System: Renin, Angiotensin, and Aldosterone
2 Comparative Aspects
3 Brief Overview of the Renin‐Angiotensin‐Aldosterone System
4 Biochemistry and Molecular Biology of the Renin System
4.1 Prorenin
4.2 Renin
4.3 Renin Substrate
4.4 Angiotensins I and II
4.5 Angiotensin‐Converting Enzyme
4.6 Aldosterone
4.7 Methods of Measurement
5 Physiology
5.1 Prorenin
5.2 Renin
5.3 Renin Substrate
5.4 Angiotensin II
5.5 Aldosterone
6 Cybernetics of the System
6.1 Coordinated Regulation of Sodium, Potassium, and Blood Pressure
7 Use of the Renin System to Understand Blood Pressure Control and Disorders of Pressure‐Volume Homeostasis
7.1 Two Forms of Vasoconstriction: Vasoconstriction‐Volume Analysis
7.2 Three Basic Tenets Concerning Plasma Renin Measurements
7.3 The Sodium—Calcium Connection
7.4 Dynamic Reciprocity of Two Forms of Vasoconstriction
7.5 The Sympathetic Nervous System and Modulation of the Two Forms of Arteriolar Vasoconstriction
8 Human Disorders of the Renin System
8.1 Hypertensive Disorders
8.2 Renin System Abnormalities in Edematous States
8.3 Hypokalemic Normotensive States
9 Summary
Figure 1. Figure 1.

Renin‐angiotensin‐aldosterone system. Renin, secreted in response to reduced arterial pressure or reduced renal tubular sodium, cleaves angiotensin I from circulating angiotensinogen (renin substrate). Angiotensin‐converting enzyme (ACE) then converts angiotensin I to angiotensin II. Angiotensin II raises pressure by direct arteriolar vasoconstriction and stimulates adrenal aldosterone secretion; together, aldosterone and angiotensin II cause renal sodium retention. Resultant fluid accumulation leads to improved flow. These pressure and volume effects in turn lead to suppression of renin release. Dashed line indicates negative feedback.

From Laragh et al.
Figure 2. Figure 2.

Amino acid sequence of human preprorenin. Asp38 and Asp226 are the two aspartic acids involved in catalysis. Large arrows are likely sites of hydrolysis of signal peptide and prosequence.

From Morris et al.
Figure 3. Figure 3.

Relation of renin activity in plasma samples obtained at noon, and of corresponding 24 h urinary excretion of aldosterone, to concurrent daily rate of sodium excretion. For these normal subjects, data describe dynamic hyperbolic relationship between each hormone and sodium excretion. Dynamic fluctuations in renin in response to changes in sodium intake help to maintain blood pressure constant during wide changes in sodium balance. Renin and aldosterone responses work together in kidney to conserve or eliminate sodium in response to changes in dietary sodium intake. Of note is that subjects studied on random diets outside the hospital or while on carefully controlled diets in the hospital exhibited similar relationships–a finding that validates use of this nomogram in studying outpatients or subjects not receiving constant diets.

Laragh et al.
Figure 4. Figure 4.

Relationship of renal vein renin to arterial renin in patients with essential hypertension. (Peripheral venous, infrarenal inferior vena caval, and arterial renin levels are identical and interchangeable in this relationship.) Dashed line is described by loge renal vein renin = 1.24 + 1.02 loge arterial renin. Slope of the line is not different from line of identity, indicating that relationship of renal vein renin to arterial renin is constant at all levels of plasma renin activity found in essential hypertension. Intercept of 1.24 indicates that renal vein renin is 124% of arterial renin. AI, angiotensin I.

From Sealey et al.
Figure 5. Figure 5.

Equations illustrating how renal plasma flow can be roughly calculated in human subjects from renal vein renin (V) and peripheral venous, infrarenal inferior vena caval, or arterial (A) renin measurements. Equations are especially useful in diagnosis of unilateral renovascular hypertension when renin is secreted from only one kidney (see later under Renovascular Hypertension).

From Sealey et al.
Figure 6. Figure 6.

Response of arterial blood pressure (BP) to intravenous injection (arrow) of renin (R) and angiotensin (A). It can be seen in an animal model that pressor response to renin is delayed and prolonged relative to that of angiotensin because it is a consequence of enzymatic generation of angiotensin II, which has immediate and short‐lived pressor action.

Lee et al.
Figure 7. Figure 7.

Effect of differences in renin substrate concentration on rate of generation of angiotensin. There was no difference in rate when undiluted plasma samples exhibiting various angiotensinogen concentrations were compared with various dilutions of plasma that had endogenously high renin substrate. These samples were obtained at various times during oral contraceptive administration. Normal substrate concentration is ∼1,800 ng/ml. Data suggest that concentration of angiotensinogen in human plasma is normally rate limiting. They also suggest that observed differences in rate of angiotensin generation are related to differences in renin substrate concentration and not to variations in concentration of activator or inhibitor of renin.

From Newton et al.
Figure 8. Figure 8.

Steps in processing and degradation of angiotensin. Converting enzyme activity probably occurs primarily in pulmonary circulation, but is also present on vascular endothelial cells and in blood.

From Gocke et al.
Figure 9. Figure 9.

Biosynthetic pathways from cholesterol to mineralocorticoids (aldosterone), glucocorticoids (cortisol), and androgens (androstenedione) are shown, as are structures of cholesterol, aldosterone, cortisol, and androstenedione (small amounts of testosterone and estrogen are also synthesized in adrenal gland). Positions 3, 11, 17, 18, and 21 are marked on diagram of a steroid molecule (bottom right), Arrows indicate individual biosynthetic conversions. Enzyme specifically mediating each step is indicated at top or left, with name of enzymatic activity in parentheses; note that one protein can mediate more than one step. OH hydroxyl and CMO corticosterone methyl oxidase.

From White et al.
Figure 10. Figure 10.

Relationship, on log‐log scale, of 24 h urine potassium excretion to 24 h excretion of acidlabile conjugate of aldosterone. Data are from longitudinal study of 254 normal subjects evaluated once a year for 4–9 years. Each point represents data from randomly collected urine sample. Ranges of sodium and potassium excretions reflect normal differences in dietary habits, except that in 1 year 144 of the subjects were asked to restrict their sodium intake moderately. Panels reflect three different ranges of sodium. Relationships between urine potassium and urine aldosterone are described by equations log aldo = 1.21 log UKV‐1.17 (UNaV<80), R = 0.70, P<.001; log aldo = 0.89 log UKV‐0.76 (UNaV 80–150) R = 0.55, P<.001; log aldo = 0.69 log UKV‐0.52 (UNaV>150 mEq/day), R = 0.45, P<.001.

From James et al., unpublished data
Figure 11. Figure 11.

Relationship between plasma active renin and proportion of plasma inactive renin (prorenin). Large circles labeled A, B, and C represent three patients with ectopic renin‐secreting tumors. Small closed circles represent normal subjects; open symbols, essential hypertensive patients with low (□), normal (○), or high (Δ) renin‐sodium profiles. ▪, Primary aldosteronism; ▴, malignant or renovascular hypertension; a, adrenal cortical insufficiency; b, Bartter's syndrome; c, hepatic cirrhosis; g, ganglioneuroma; t, trophoblastic disease. Absolute levels of renin and prorenin in these patients are published in Atlas et al. .

From Atlas et al.
Figure 12. Figure 12.

Hormonal changes throughout menstrual cycle in one normal woman. Day zero = LH (luteinizing hormone) peak; FSH, follicle‐stimulating hormone. Note that peak of prorenin immediately follows LH surge and is not accompanied by change in active renin.

From Sealey et al.
Figure 13. Figure 13.

Juxtaglomerular apparatus of rat, illustrating tubular and vascular components. Tubular component consists of specialized region of thick ascending limb of Henle–macula densa (MD). This can be identified by close proximity of nuclei of these cells to each other. Vascular component consists of afferent (A) and efferent (E) arterioles and extraglomerular mesangium (EM; also known as “lacis,” “group of cells of Goormaghtigh,” and “polkissen”). MD is in contact with EM. EM is continuous with intraglomerular mesangium (IM). Granular cells (GC) are seen in walls of glomerular arterioles and are most abundant in afferent arteriole, but positive cells can occur in IM and efferent arterioles. Vascular and tubular components are innervated by sympathetic nerves (N). B, Bowman's space; G, glomerular capillary.

From Barajas
Figure 14. Figure 14.

Hypothetical renin‐containing juxtaglomerular cell plasma membrane. Sodium–calcium exchange carrier binds Na+ and Ca2+ in 3:1 ratio. In presence of normal transmembrane Na+ electrochemical gradient, Na+ influx down its gradient is coupled with Ca2+ efflux against its gradient; decreases in Na+ electrochemical gradient (caused by membrane depolarization, increased , or decreased ) decrease rate of Ca2+ efflux and conversely. Transmembrane Na+ and K+ concentration gradients, and ultimately transmembrane potential, are maintained by primary active transport of Na+ and K+ (Na+,K+‐ATPase).

From Churchill
Figure 15. Figure 15.

Time course of renin release from single perfused juxtaglomerular apparatus (JGA). Top: time course of renin secretion from six JGA perfused with control solution throughout experiments. After 50 min a mock perfusate change was made. Bottom: time course of renin secretion from six JGA perfused with control solution for initial 50 min (closed circles), after which perfusate was changed to low NaCl isosmotic solution (open circles). Values given are arithmetic means; bars show SEM. In upper panel, mean renin release rate did not differ between control and experimental periods, whereas in lower panel a significant increase occurred in the experimental period relative to control (P<0.01, paired t test). Asterisks indicate P values for comparison of individual time periods with corresponding periods in time control series (*P<0.05, **P<0.02).

From Skøtt and Briggs
Figure 16. Figure 16.

Effect of 30 min of 65° head‐up tilt in normal subjects before and after 0.12 mg/kg intravenous propranolol HCI during high sodium (200 mEq/day) and low sodium (10 mEq/day) intakes. When renin increase in response to tilt was blocked by propranolol during high sodium intake, blood pressure was not compromised (left panel). This was in contrast to effect on low sodium intake where the baseline renin was higher and response of renin to tilt was greater (right panel). When this response was blocked by propranolol, blood pressure fell dramatically. This study illustrates importance of renin system in maintaining blood pressure during sodium depletion and upright posture.

From Morganti et al.
Figure 17. Figure 17.

Hormonal changes in one young woman during two 24 h periods separated by 1 week. Dietary intake on each day was 100 mEq/day sodium, 60 mEq/day potassium. Left: subject was supine for 23 h, from 9 A.M. to 8 A.M. the following day. Right: subject went about her daily work and was supine only from 11 P.M. to 8 A.M. During continuously supine day, atrial natriuretic factor (ANF) increased at start of bed rest and then gradually fell, reaching its lowest level from 9 P.M. to 3 A.M. It rose again between 6 and 8 A.M. There was no apparent effect of ANF on aldosterone to renin relationships (UA/PRA). During ambulatory/supine study, lowest aldosterone levels and lowest UA/PRA ratio occurred when ANF increased to >20 fmol/ml, which occurred between 12 P.M. and 6 A.M. This would be consistent with well‐known effects of ANF in vitro to suppress aldosterone response to angiotensin II stimulation. (From Bell et al., unpublished data.)

Figure 18. Figure 18.

Blood (black areas) and plasma (dotted areas) volumes, cumulative sodium balance, plasma renin activity, and daily urinary aldosterone excretion data for six normal subjects on I, normal sodium intake; IV, after sodium depletion and consequent blood volume reduction; V, during sodium repletion without volume repletion; and VI, during volume repletion without concurrent increase in sodium balance. Volume expansion was prevented during period V by serial bleedings. Plasma renin activity fell during sodium repletion (period V) despite fall in total blood volume in all subjects. Renin therefore appears to respond to sodium and not to total blood volume.

From Bull et al.
Figure 19. Figure 19.

Prolonged continuous angiotensin infusion in normal subject for 11 days. Dose of angiotensin was adjusted to maintain mildly pressor response. Angiotensin II induced marked and selective increase in adrenal cortical secretion of aldosterone. Together with direct effect of angiotensin II on proximal tubule sodium reabsorption, rise in aldosterone caused sodium retention. As sodium was retained, angiotensin became more pressor. Because of this increasing pressor sensitivity to angiotensin, dose of angiotensin II had to be serially reduced to maintain same level of blood pressure. Consequently, aldosterone secretion fell to close to control levels. Thus pressor sensitivity to angiotensin increased as sodium retention progressed. Results indicate angiotensin, unlike norepinephrine, can produce and then sustain hypertension in progressively smaller amounts as sodium‐volume gain turns off need for angiotensin.

From Laragh et al.
Figure 20. Figure 20.

Effect of angiotensin II on aldosterone secretion in eight normal subjects. In all eight experiments infusion of angiotensin II caused significant increase in adrenal secretory rate of aldosterone as compared with control infusion of isotonic glucose. Urinary sodium excretion usually decreased with angiotensin, a finding consistent with increased aldosterone production and a direct renal effect of angiotensin II.

From Laragh et al.
Figure 21. Figure 21.

Study of effect of increased potassium administration for 5 days in normal subject maintained on constant dietary sodium regimen. Plasma renin activity (PRA) was serially suppressed as urinary aldosterone and urinary sodium and potassium increased. Closed circles are plasma Na+ and plasma K+.

From Brunner et al.
Figure 22. Figure 22.

Effect of potassium administration on aldosterone secretion of two patients with renal tubule disease. Large changes in aldosterone secretion rate occurred in response to increased potassium intake (solid bars) when patients received normal sodium diet. Potassium administration during sodium depletion induced even greater hypersecretion of aldosterone. In both studies serum potassium concentration increased but did not exceed normal levels.

From Cannon et al.
Figure 23. Figure 23.

Effect of intramuscular administration of ACTH, 40 U b.i.d., in normal subject. ACTH increased aldosterone excretion much more during sodium depletion (left) than during normal sodium intake (right). However, response to ACTH was not sustained during 5 days of administration on either sodium intake, and aldosterone actually fell below baseline levels when injections were terminated during sodium deprivation and while ACTH was administered during normal sodium intake.

From Newton and Laragh
Figure 24. Figure 24.

Renin system in normal subjects divided according to blood pressure and plasma renin levels. Analysis was carried out in 139 normal subjects divided into normotensive [n = 99, solid boxes and lines; diastolic blood pressure (DBP) < 85 mm Hg] and borderline hypertensive groups (n = 40, dashed boxes and lines; DBP 85–100 mm Hg). Each blood pressure group was subdivided on basis of renin level into low (<1 ng/ml/h, n = 14, 7), medium (1–5 ng/ml/h, n = 77, 26), or high (>5 ng/ml/h, n = 8, 7) renin groups. As expected, urine and plasma aldosterone followed renin levels. Nonetheless, differences in aldosterone between groups were not as great on a percentage basis; nor were they always statistically significant. Urine aldosterone to renin ratio (UA/PRA) was highest in both low renin groups and lowest in both high renin groups. This could not be ascribed to effect of potassium to stimulate aldosterone, because low renin groups did not have higher urine or serum potassium. Low renin subjects seem to have increased adrenal sensitivity to angiotensin II, but basis for this is unexplained.

From Sealey et al., unpublished data
Figure 25. Figure 25.

Illustration of link between sodium balance and blood pressure homeostasis and between sodium balance and potassium homeostasis. However, there is little evidence for link between potassium and blood pressure.

Figure 26. Figure 26.

Data from Figure replotted to illustrate mean urinary sodium excretion for given ranges of plasma renin activity and urinary aldosterone excretion. Differences in sodium excretion are significant at all higher rates suggesting that angiotensin and aldosterone continue to exert regulatory effect on urinary sodium excretion even when circulating concentrations are low.

From Laragh et al.
Figure 27. Figure 27.

Periodic fluctuations in urine sodium excretion, sodium balance, plasma renin activity, and urine aldosterone excretion after initiation of high sodium diet (270 mEq), which was preceded by 11 days of sodium deprivation (10 mEq/day) (not shown here; see Fig. ). Mean values ±SD from three normal subjects are presented. Each subject exhibited similar periodic fluctuation in urine sodium, renin, and aldosterone. After 4 days of diet, natriuresis occurred for 3 days, and these high levels of sodium excretion were associated with lowest levels of plasma renin activity and aldosterone excretion.

From Sealey et al.
Figure 28. Figure 28.

Demonstration that when angiotensin II is fixed during changes in sodium intake, blood pressure increases with sodium loading and is at its lowest level with sodium depletion. Changes in mean arterial pressure during chronic changes in sodium intake in control dogs and in dogs during angiotensin II blockade with the converting enzyme inhibitor SQ 14.225 or during angiotensin II infusion (5 mg‐kg−1.min) also shown. Values are means ±SE.

From Hall et al.
Figure 29. Figure 29.

Top: interrelationship of renin‐aldosterone hormonal system with changes in sodium and potassium balance. Bottom: coordination of intrarenal physical factors with hormonal factors for sodium and potassium homeostasis. Rate of excretion of each cation is determined by interaction of aldosterone with distal tubular sodium supply.

From Sealey and Laragh
Figure 30. Figure 30.

Effect of sodium depletion on urine aldosterone excretion and potassium balance–combined results from five normal subjects. Despite hyperaldosteronism induced by sodium depletion, potassium balance became progressively positive. Therefore, other factors (see Fig. ) counterbalance kaliuretic action of aldosterone. Increase in aldosterone‐renin ratio most likely reflects gradual increase in potassium balance; this change was accompanied by only modest increases in plasma potassium.

From Laragh et al.
Figure 31. Figure 31.

Acute effects (at 90 min) of two different converting enzyme inhibitors, teprotide and captopril, on diastolic blood pressure. With both drugs, percent fall in blood pressure is closely related to pretreatment levels of plasma renin activity in quietly seated, untreated hypertensive patients. Note also that almost every subject exhibited some hypotensive response to drug, again illustrating (see Fig. ) that even low levels of renin may have an effect. Left: effects of administering nonapeptide (isolated from snake venom) teprotide (SQ 20881), intravenously to 89 patients; data are replotted from Case et al. . Right: changes in seated diastolic blood pressure 90 min after single oral dose of 25 mg captopril to 166 patients; data are replotted from Case et al. and Laragh et al. . Setting aside errors in cuff pressure measurements, data reveal remarkable and extremely similar correlations between height of pretreatment plasma renin value and degree of induced decrease in blood pressure. Note that patients with plasma renin values <1.0 ng/ml/h exhibited smallest change in pressure. Both sets of data also provide strong indirect evidence that plasma renin value reflects active role of renin in supporting arterial pressure in hypertensive persons.

Data replotted from Case et al. and Laragh et al.
Figure 32. Figure 32.

Relationship between acute (60 min) fall in diastolic pressure and baseline renin in response to oral captopril (25–50 mg) in group of hypertensive patients divided into those with 30 min seated renins of <1, 1–6, or >6 ng/ml/h. The higher the baseline renin of each group, the greater the fall in diastolic pressure. On average, captopril lowered diastolic pressure by close to 20 mm Hg in the 74 high renin patients; fall was only 5 mm Hg in low renin group.

From Mueller et al.
Figure 33. Figure 33.

Serum levels of magnesium (left) and ionized calcium (right) in normotensive control subjects (N1 BP) and in different renin subgroups of essential hypertensive subjects. Low, medium, and high renin essential hypertension abbreviated as Lo RH, N1 RH, and Hi RH, respectively. For both cations, hypertensive patients differ significantly from normotensive controls. To convert to millimoles per liter, multiply by 0.5.

From Resnick et al.
Figure 34. Figure 34.

Relationship of the percent fall in systolic pressure during treatment with verapamil (120 mg, 3xday) to baseline ambulatory plasma renin activity in 13 hypertensive patients. Patients represented by circles were on low‐sodium intake (9 mEq/day); those represented by triangles were on a high‐sodium intake (212 mEq/day). Those on high‐sodium intake and those with lower plasma renin levels were more responsive to the calcium channel blocker.

From Nicholson et al.
Figure 35. Figure 35.

Cellular calcium hypothesis of hypertension that reconciles observed heterogeneous extracellular divalent cation levels among hypertensive patients with their presumed uniformly abnormal intracellular concentrations, ex, Extracellular calcium; cyt, cytosolic free calcium; BP, blood pressure.

From Resnick
Figure 36. Figure 36.

In two‐kidney, one‐clip renal hypertensive rats infusion of angiotensin receptor antagonist saralasin induced immediate fall in blood pressure, which reached −40.8±4.2 mm Hg after 60 min (P<0.001). In contrast, change in blood pressure induced in one‐kidney, one‐clip renal hypertensive rats was not significant (P>0.1).

From Brunner et al.
Figure 37. Figure 37.

In sodium‐depleted, one‐kidney, one‐clip renovascular hypertensive rats, infusion of angiotensin II antagonist saralasin produced striking falls in blood pressure. Twenty‐four hours later, after same animals were sodium repleted, there was no significant effect on blood pressure by same dose of antagonist. These studies illustrate dynamic relationship between sodium and renin in maintaining elevated blood pressure of this form of renovascular hypertension

From Gavras et al.
Figure 38. Figure 38.

Illustration that blood pressure reduction induced by angiotensin II blockade can be reversed by sodium loading in patient with malignant hypertension (studied under balance ward conditions). First vasoconstriction and then volume support to hypertension are shown. Angiotensin blockade with saralasin produced dramatic fall in blood pressure. However, as blockade was maintained, when sodium chloride was infused over next 40 h, blood pressure returned to high control values and excess volume replaced vasoconstriction in support of blood pressure. Administration of 40 mg Lasix (L40) during continued angiotensin II blockade resulted in diuresis and fall in blood pressure.

From Brunner et al.
Figure 39. Figure 39.

Metabolism balance study of patient with pseudoprimary aldosteronism. Dotted lines indicate intakes of potassium and sodium. Normal ranges for aldosterone secretion and for midday serum renin in ambient subjects for each dietary sodium intake are indicated by range bars. Aldosterone secretion was always markedly elevated, and serum renin levels were abnormally low. Responses of aldosterone and renin to manipulations in sodium intake were blunted. Potassium repletion was more easily accomplished when dietary sodium was reduced.

From Ledingham et al.
Figure 40. Figure 40.

Renal–adrenal axis is hormonal cascade involving renin, angiotensin, and aldosterone for regulation of sodium and potassium balance and blood pressure. Interaction is depicted as it was first discovered in studies of patients with malignant hypertension in whom, because of defective feedback, it is involved in causation. Accordingly, there is massive excess of both renin and aldosterone that cannot turn itself off.

From Laragh et al.
Figure 41. Figure 41.

Different high blood pressure mechanisms, pathophysiological changes, and treatment strategies in high and low renin hypertensive patients.

Adapted from Laragh et al.
Figure 42. Figure 42.

Different blood pressure mechanisms in two animal models of renovascular (i.e., Goldblatt) hypertension. Although comparable blood pressure elevation occurs in Goldblatt hypertension of either the one‐kidney or two‐kidney type, different mechanisms are involved. Volume overexpansion from impaired renal excretory capacity is implicated in one‐kidney type, whereas renin‐initiated vasoconstriction appears largely responsible for two‐kidney type.

From Laragh et al.
Figure 43. Figure 43.

Dramatic difference in 60‐min plasma renin response to single oral dose of converting enzyme inhibitor captopril between patients with essential hypertension and those with renovascular disease. Response is used as basis of screening test for renovascular hypertension.

From Mueller et al.
Figure 44. Figure 44.

Renal angioplasty reduces plasma renin activity into normal range in patients with renovascular hypertension. Left: before angioplasty; right: 6 months after angioplasty. Hatched area shows normal range of plasma renin in relation to concurrent 24 h urine sodium excretion.

From Pickering et al.
Figure 45. Figure 45.

Renal vein renin diagnostic patterns. In essential hypertension (top), renin level in each renal vein is ∼25% greater than peripheral arterial, venous, or infrarenal inferior vena caval renin at all levels of renin secretion. In setting of unilateral renin secretion (curable renovascular hypertension; bottom left), affected kidney is solely responsible for maintaining peripheral renin levels. Hence, increment is at least 50% (0.5) and becomes progressively greater as renal blood flow is reduced. Patients with unilateral secretion of renin and normal BUN and'serum creatinine can usually be cured by angioplasty, surgical repair, or nephrectomy. But, if BUN and serum creatinine are elevated, bilateral disease is likely, even if contralateral suppression of renin secretion is observed. Unequal bilateral renin secretion (bottom right) indicates bilateral disease and decreases change of cure following unilateral nephrectomy, but improvement or even cure may be possible following angioplasty or corrective surgery. V1, renal vein renin; V2, renal vein renin on opposite side; IVC, inferior vena caval renin. Bold face large numbers indicate levels of plasma renin at the sites indicated.

From Laragh & Seale
Figure 46. Figure 46.

Relation of noon ambulatory plasma renin activity (left) and corresponding daily urinary aldosterone excretion (right) to concurrent daily rate of urinary sodium excretion. Dashed lines outline normal channel derived from study of normotensive people (see Fig. ). Total of 219 patients with untreated essential hypertension were studied, some on several occasions and at different levels of sodium intake. Three major subgroups (▴, low renin, ○, normal renin, and ▪, high renin essential hypertension) are defined by appropriateness or normalcy of plasma renin activity to rate of sodium excretion, used as index of dietary intake. Additional abnormal subgroups are defined when aldosterone (right) is included in the analysis.

From Brunner et al.
Figure 47. Figure 47.

Response to intravenous converting enzyme inhibition (MK 422) based on specific mechanisms of vasoconstriction. Left: High renin heart failure patient has prompt hemodynamic improvement following small dose of intravenous enalaprilat with further improvement in repeat challenge. Right: Low renin patient with comparable heart failure did not respond to intravenous enalaprilat but had prompt response to oral calcium channel inhibitor nifedipine (10 mg). Findings are representative of relative selectivity of response based on the mechanism of vasoconstriction. MAP, mean arterial pressure; PCWP, pulmonary capillary wedge pressure; CI, cardiac index; SVR, systemic vascular resistance.

From Cody et al.


Figure 1.

Renin‐angiotensin‐aldosterone system. Renin, secreted in response to reduced arterial pressure or reduced renal tubular sodium, cleaves angiotensin I from circulating angiotensinogen (renin substrate). Angiotensin‐converting enzyme (ACE) then converts angiotensin I to angiotensin II. Angiotensin II raises pressure by direct arteriolar vasoconstriction and stimulates adrenal aldosterone secretion; together, aldosterone and angiotensin II cause renal sodium retention. Resultant fluid accumulation leads to improved flow. These pressure and volume effects in turn lead to suppression of renin release. Dashed line indicates negative feedback.

From Laragh et al.


Figure 2.

Amino acid sequence of human preprorenin. Asp38 and Asp226 are the two aspartic acids involved in catalysis. Large arrows are likely sites of hydrolysis of signal peptide and prosequence.

From Morris et al.


Figure 3.

Relation of renin activity in plasma samples obtained at noon, and of corresponding 24 h urinary excretion of aldosterone, to concurrent daily rate of sodium excretion. For these normal subjects, data describe dynamic hyperbolic relationship between each hormone and sodium excretion. Dynamic fluctuations in renin in response to changes in sodium intake help to maintain blood pressure constant during wide changes in sodium balance. Renin and aldosterone responses work together in kidney to conserve or eliminate sodium in response to changes in dietary sodium intake. Of note is that subjects studied on random diets outside the hospital or while on carefully controlled diets in the hospital exhibited similar relationships–a finding that validates use of this nomogram in studying outpatients or subjects not receiving constant diets.

Laragh et al.


Figure 4.

Relationship of renal vein renin to arterial renin in patients with essential hypertension. (Peripheral venous, infrarenal inferior vena caval, and arterial renin levels are identical and interchangeable in this relationship.) Dashed line is described by loge renal vein renin = 1.24 + 1.02 loge arterial renin. Slope of the line is not different from line of identity, indicating that relationship of renal vein renin to arterial renin is constant at all levels of plasma renin activity found in essential hypertension. Intercept of 1.24 indicates that renal vein renin is 124% of arterial renin. AI, angiotensin I.

From Sealey et al.


Figure 5.

Equations illustrating how renal plasma flow can be roughly calculated in human subjects from renal vein renin (V) and peripheral venous, infrarenal inferior vena caval, or arterial (A) renin measurements. Equations are especially useful in diagnosis of unilateral renovascular hypertension when renin is secreted from only one kidney (see later under Renovascular Hypertension).

From Sealey et al.


Figure 6.

Response of arterial blood pressure (BP) to intravenous injection (arrow) of renin (R) and angiotensin (A). It can be seen in an animal model that pressor response to renin is delayed and prolonged relative to that of angiotensin because it is a consequence of enzymatic generation of angiotensin II, which has immediate and short‐lived pressor action.

Lee et al.


Figure 7.

Effect of differences in renin substrate concentration on rate of generation of angiotensin. There was no difference in rate when undiluted plasma samples exhibiting various angiotensinogen concentrations were compared with various dilutions of plasma that had endogenously high renin substrate. These samples were obtained at various times during oral contraceptive administration. Normal substrate concentration is ∼1,800 ng/ml. Data suggest that concentration of angiotensinogen in human plasma is normally rate limiting. They also suggest that observed differences in rate of angiotensin generation are related to differences in renin substrate concentration and not to variations in concentration of activator or inhibitor of renin.

From Newton et al.


Figure 8.

Steps in processing and degradation of angiotensin. Converting enzyme activity probably occurs primarily in pulmonary circulation, but is also present on vascular endothelial cells and in blood.

From Gocke et al.


Figure 9.

Biosynthetic pathways from cholesterol to mineralocorticoids (aldosterone), glucocorticoids (cortisol), and androgens (androstenedione) are shown, as are structures of cholesterol, aldosterone, cortisol, and androstenedione (small amounts of testosterone and estrogen are also synthesized in adrenal gland). Positions 3, 11, 17, 18, and 21 are marked on diagram of a steroid molecule (bottom right), Arrows indicate individual biosynthetic conversions. Enzyme specifically mediating each step is indicated at top or left, with name of enzymatic activity in parentheses; note that one protein can mediate more than one step. OH hydroxyl and CMO corticosterone methyl oxidase.

From White et al.


Figure 10.

Relationship, on log‐log scale, of 24 h urine potassium excretion to 24 h excretion of acidlabile conjugate of aldosterone. Data are from longitudinal study of 254 normal subjects evaluated once a year for 4–9 years. Each point represents data from randomly collected urine sample. Ranges of sodium and potassium excretions reflect normal differences in dietary habits, except that in 1 year 144 of the subjects were asked to restrict their sodium intake moderately. Panels reflect three different ranges of sodium. Relationships between urine potassium and urine aldosterone are described by equations log aldo = 1.21 log UKV‐1.17 (UNaV<80), R = 0.70, P<.001; log aldo = 0.89 log UKV‐0.76 (UNaV 80–150) R = 0.55, P<.001; log aldo = 0.69 log UKV‐0.52 (UNaV>150 mEq/day), R = 0.45, P<.001.

From James et al., unpublished data


Figure 11.

Relationship between plasma active renin and proportion of plasma inactive renin (prorenin). Large circles labeled A, B, and C represent three patients with ectopic renin‐secreting tumors. Small closed circles represent normal subjects; open symbols, essential hypertensive patients with low (□), normal (○), or high (Δ) renin‐sodium profiles. ▪, Primary aldosteronism; ▴, malignant or renovascular hypertension; a, adrenal cortical insufficiency; b, Bartter's syndrome; c, hepatic cirrhosis; g, ganglioneuroma; t, trophoblastic disease. Absolute levels of renin and prorenin in these patients are published in Atlas et al. .

From Atlas et al.


Figure 12.

Hormonal changes throughout menstrual cycle in one normal woman. Day zero = LH (luteinizing hormone) peak; FSH, follicle‐stimulating hormone. Note that peak of prorenin immediately follows LH surge and is not accompanied by change in active renin.

From Sealey et al.


Figure 13.

Juxtaglomerular apparatus of rat, illustrating tubular and vascular components. Tubular component consists of specialized region of thick ascending limb of Henle–macula densa (MD). This can be identified by close proximity of nuclei of these cells to each other. Vascular component consists of afferent (A) and efferent (E) arterioles and extraglomerular mesangium (EM; also known as “lacis,” “group of cells of Goormaghtigh,” and “polkissen”). MD is in contact with EM. EM is continuous with intraglomerular mesangium (IM). Granular cells (GC) are seen in walls of glomerular arterioles and are most abundant in afferent arteriole, but positive cells can occur in IM and efferent arterioles. Vascular and tubular components are innervated by sympathetic nerves (N). B, Bowman's space; G, glomerular capillary.

From Barajas


Figure 14.

Hypothetical renin‐containing juxtaglomerular cell plasma membrane. Sodium–calcium exchange carrier binds Na+ and Ca2+ in 3:1 ratio. In presence of normal transmembrane Na+ electrochemical gradient, Na+ influx down its gradient is coupled with Ca2+ efflux against its gradient; decreases in Na+ electrochemical gradient (caused by membrane depolarization, increased , or decreased ) decrease rate of Ca2+ efflux and conversely. Transmembrane Na+ and K+ concentration gradients, and ultimately transmembrane potential, are maintained by primary active transport of Na+ and K+ (Na+,K+‐ATPase).

From Churchill


Figure 15.

Time course of renin release from single perfused juxtaglomerular apparatus (JGA). Top: time course of renin secretion from six JGA perfused with control solution throughout experiments. After 50 min a mock perfusate change was made. Bottom: time course of renin secretion from six JGA perfused with control solution for initial 50 min (closed circles), after which perfusate was changed to low NaCl isosmotic solution (open circles). Values given are arithmetic means; bars show SEM. In upper panel, mean renin release rate did not differ between control and experimental periods, whereas in lower panel a significant increase occurred in the experimental period relative to control (P<0.01, paired t test). Asterisks indicate P values for comparison of individual time periods with corresponding periods in time control series (*P<0.05, **P<0.02).

From Skøtt and Briggs


Figure 16.

Effect of 30 min of 65° head‐up tilt in normal subjects before and after 0.12 mg/kg intravenous propranolol HCI during high sodium (200 mEq/day) and low sodium (10 mEq/day) intakes. When renin increase in response to tilt was blocked by propranolol during high sodium intake, blood pressure was not compromised (left panel). This was in contrast to effect on low sodium intake where the baseline renin was higher and response of renin to tilt was greater (right panel). When this response was blocked by propranolol, blood pressure fell dramatically. This study illustrates importance of renin system in maintaining blood pressure during sodium depletion and upright posture.

From Morganti et al.


Figure 17.

Hormonal changes in one young woman during two 24 h periods separated by 1 week. Dietary intake on each day was 100 mEq/day sodium, 60 mEq/day potassium. Left: subject was supine for 23 h, from 9 A.M. to 8 A.M. the following day. Right: subject went about her daily work and was supine only from 11 P.M. to 8 A.M. During continuously supine day, atrial natriuretic factor (ANF) increased at start of bed rest and then gradually fell, reaching its lowest level from 9 P.M. to 3 A.M. It rose again between 6 and 8 A.M. There was no apparent effect of ANF on aldosterone to renin relationships (UA/PRA). During ambulatory/supine study, lowest aldosterone levels and lowest UA/PRA ratio occurred when ANF increased to >20 fmol/ml, which occurred between 12 P.M. and 6 A.M. This would be consistent with well‐known effects of ANF in vitro to suppress aldosterone response to angiotensin II stimulation. (From Bell et al., unpublished data.)



Figure 18.

Blood (black areas) and plasma (dotted areas) volumes, cumulative sodium balance, plasma renin activity, and daily urinary aldosterone excretion data for six normal subjects on I, normal sodium intake; IV, after sodium depletion and consequent blood volume reduction; V, during sodium repletion without volume repletion; and VI, during volume repletion without concurrent increase in sodium balance. Volume expansion was prevented during period V by serial bleedings. Plasma renin activity fell during sodium repletion (period V) despite fall in total blood volume in all subjects. Renin therefore appears to respond to sodium and not to total blood volume.

From Bull et al.


Figure 19.

Prolonged continuous angiotensin infusion in normal subject for 11 days. Dose of angiotensin was adjusted to maintain mildly pressor response. Angiotensin II induced marked and selective increase in adrenal cortical secretion of aldosterone. Together with direct effect of angiotensin II on proximal tubule sodium reabsorption, rise in aldosterone caused sodium retention. As sodium was retained, angiotensin became more pressor. Because of this increasing pressor sensitivity to angiotensin, dose of angiotensin II had to be serially reduced to maintain same level of blood pressure. Consequently, aldosterone secretion fell to close to control levels. Thus pressor sensitivity to angiotensin increased as sodium retention progressed. Results indicate angiotensin, unlike norepinephrine, can produce and then sustain hypertension in progressively smaller amounts as sodium‐volume gain turns off need for angiotensin.

From Laragh et al.


Figure 20.

Effect of angiotensin II on aldosterone secretion in eight normal subjects. In all eight experiments infusion of angiotensin II caused significant increase in adrenal secretory rate of aldosterone as compared with control infusion of isotonic glucose. Urinary sodium excretion usually decreased with angiotensin, a finding consistent with increased aldosterone production and a direct renal effect of angiotensin II.

From Laragh et al.


Figure 21.

Study of effect of increased potassium administration for 5 days in normal subject maintained on constant dietary sodium regimen. Plasma renin activity (PRA) was serially suppressed as urinary aldosterone and urinary sodium and potassium increased. Closed circles are plasma Na+ and plasma K+.

From Brunner et al.


Figure 22.

Effect of potassium administration on aldosterone secretion of two patients with renal tubule disease. Large changes in aldosterone secretion rate occurred in response to increased potassium intake (solid bars) when patients received normal sodium diet. Potassium administration during sodium depletion induced even greater hypersecretion of aldosterone. In both studies serum potassium concentration increased but did not exceed normal levels.

From Cannon et al.


Figure 23.

Effect of intramuscular administration of ACTH, 40 U b.i.d., in normal subject. ACTH increased aldosterone excretion much more during sodium depletion (left) than during normal sodium intake (right). However, response to ACTH was not sustained during 5 days of administration on either sodium intake, and aldosterone actually fell below baseline levels when injections were terminated during sodium deprivation and while ACTH was administered during normal sodium intake.

From Newton and Laragh


Figure 24.

Renin system in normal subjects divided according to blood pressure and plasma renin levels. Analysis was carried out in 139 normal subjects divided into normotensive [n = 99, solid boxes and lines; diastolic blood pressure (DBP) < 85 mm Hg] and borderline hypertensive groups (n = 40, dashed boxes and lines; DBP 85–100 mm Hg). Each blood pressure group was subdivided on basis of renin level into low (<1 ng/ml/h, n = 14, 7), medium (1–5 ng/ml/h, n = 77, 26), or high (>5 ng/ml/h, n = 8, 7) renin groups. As expected, urine and plasma aldosterone followed renin levels. Nonetheless, differences in aldosterone between groups were not as great on a percentage basis; nor were they always statistically significant. Urine aldosterone to renin ratio (UA/PRA) was highest in both low renin groups and lowest in both high renin groups. This could not be ascribed to effect of potassium to stimulate aldosterone, because low renin groups did not have higher urine or serum potassium. Low renin subjects seem to have increased adrenal sensitivity to angiotensin II, but basis for this is unexplained.

From Sealey et al., unpublished data


Figure 25.

Illustration of link between sodium balance and blood pressure homeostasis and between sodium balance and potassium homeostasis. However, there is little evidence for link between potassium and blood pressure.



Figure 26.

Data from Figure replotted to illustrate mean urinary sodium excretion for given ranges of plasma renin activity and urinary aldosterone excretion. Differences in sodium excretion are significant at all higher rates suggesting that angiotensin and aldosterone continue to exert regulatory effect on urinary sodium excretion even when circulating concentrations are low.

From Laragh et al.


Figure 27.

Periodic fluctuations in urine sodium excretion, sodium balance, plasma renin activity, and urine aldosterone excretion after initiation of high sodium diet (270 mEq), which was preceded by 11 days of sodium deprivation (10 mEq/day) (not shown here; see Fig. ). Mean values ±SD from three normal subjects are presented. Each subject exhibited similar periodic fluctuation in urine sodium, renin, and aldosterone. After 4 days of diet, natriuresis occurred for 3 days, and these high levels of sodium excretion were associated with lowest levels of plasma renin activity and aldosterone excretion.

From Sealey et al.


Figure 28.

Demonstration that when angiotensin II is fixed during changes in sodium intake, blood pressure increases with sodium loading and is at its lowest level with sodium depletion. Changes in mean arterial pressure during chronic changes in sodium intake in control dogs and in dogs during angiotensin II blockade with the converting enzyme inhibitor SQ 14.225 or during angiotensin II infusion (5 mg‐kg−1.min) also shown. Values are means ±SE.

From Hall et al.


Figure 29.

Top: interrelationship of renin‐aldosterone hormonal system with changes in sodium and potassium balance. Bottom: coordination of intrarenal physical factors with hormonal factors for sodium and potassium homeostasis. Rate of excretion of each cation is determined by interaction of aldosterone with distal tubular sodium supply.

From Sealey and Laragh


Figure 30.

Effect of sodium depletion on urine aldosterone excretion and potassium balance–combined results from five normal subjects. Despite hyperaldosteronism induced by sodium depletion, potassium balance became progressively positive. Therefore, other factors (see Fig. ) counterbalance kaliuretic action of aldosterone. Increase in aldosterone‐renin ratio most likely reflects gradual increase in potassium balance; this change was accompanied by only modest increases in plasma potassium.

From Laragh et al.


Figure 31.

Acute effects (at 90 min) of two different converting enzyme inhibitors, teprotide and captopril, on diastolic blood pressure. With both drugs, percent fall in blood pressure is closely related to pretreatment levels of plasma renin activity in quietly seated, untreated hypertensive patients. Note also that almost every subject exhibited some hypotensive response to drug, again illustrating (see Fig. ) that even low levels of renin may have an effect. Left: effects of administering nonapeptide (isolated from snake venom) teprotide (SQ 20881), intravenously to 89 patients; data are replotted from Case et al. . Right: changes in seated diastolic blood pressure 90 min after single oral dose of 25 mg captopril to 166 patients; data are replotted from Case et al. and Laragh et al. . Setting aside errors in cuff pressure measurements, data reveal remarkable and extremely similar correlations between height of pretreatment plasma renin value and degree of induced decrease in blood pressure. Note that patients with plasma renin values <1.0 ng/ml/h exhibited smallest change in pressure. Both sets of data also provide strong indirect evidence that plasma renin value reflects active role of renin in supporting arterial pressure in hypertensive persons.

Data replotted from Case et al. and Laragh et al.


Figure 32.

Relationship between acute (60 min) fall in diastolic pressure and baseline renin in response to oral captopril (25–50 mg) in group of hypertensive patients divided into those with 30 min seated renins of <1, 1–6, or >6 ng/ml/h. The higher the baseline renin of each group, the greater the fall in diastolic pressure. On average, captopril lowered diastolic pressure by close to 20 mm Hg in the 74 high renin patients; fall was only 5 mm Hg in low renin group.

From Mueller et al.


Figure 33.

Serum levels of magnesium (left) and ionized calcium (right) in normotensive control subjects (N1 BP) and in different renin subgroups of essential hypertensive subjects. Low, medium, and high renin essential hypertension abbreviated as Lo RH, N1 RH, and Hi RH, respectively. For both cations, hypertensive patients differ significantly from normotensive controls. To convert to millimoles per liter, multiply by 0.5.

From Resnick et al.


Figure 34.

Relationship of the percent fall in systolic pressure during treatment with verapamil (120 mg, 3xday) to baseline ambulatory plasma renin activity in 13 hypertensive patients. Patients represented by circles were on low‐sodium intake (9 mEq/day); those represented by triangles were on a high‐sodium intake (212 mEq/day). Those on high‐sodium intake and those with lower plasma renin levels were more responsive to the calcium channel blocker.

From Nicholson et al.


Figure 35.

Cellular calcium hypothesis of hypertension that reconciles observed heterogeneous extracellular divalent cation levels among hypertensive patients with their presumed uniformly abnormal intracellular concentrations, ex, Extracellular calcium; cyt, cytosolic free calcium; BP, blood pressure.

From Resnick


Figure 36.

In two‐kidney, one‐clip renal hypertensive rats infusion of angiotensin receptor antagonist saralasin induced immediate fall in blood pressure, which reached −40.8±4.2 mm Hg after 60 min (P<0.001). In contrast, change in blood pressure induced in one‐kidney, one‐clip renal hypertensive rats was not significant (P>0.1).

From Brunner et al.


Figure 37.

In sodium‐depleted, one‐kidney, one‐clip renovascular hypertensive rats, infusion of angiotensin II antagonist saralasin produced striking falls in blood pressure. Twenty‐four hours later, after same animals were sodium repleted, there was no significant effect on blood pressure by same dose of antagonist. These studies illustrate dynamic relationship between sodium and renin in maintaining elevated blood pressure of this form of renovascular hypertension

From Gavras et al.


Figure 38.

Illustration that blood pressure reduction induced by angiotensin II blockade can be reversed by sodium loading in patient with malignant hypertension (studied under balance ward conditions). First vasoconstriction and then volume support to hypertension are shown. Angiotensin blockade with saralasin produced dramatic fall in blood pressure. However, as blockade was maintained, when sodium chloride was infused over next 40 h, blood pressure returned to high control values and excess volume replaced vasoconstriction in support of blood pressure. Administration of 40 mg Lasix (L40) during continued angiotensin II blockade resulted in diuresis and fall in blood pressure.

From Brunner et al.


Figure 39.

Metabolism balance study of patient with pseudoprimary aldosteronism. Dotted lines indicate intakes of potassium and sodium. Normal ranges for aldosterone secretion and for midday serum renin in ambient subjects for each dietary sodium intake are indicated by range bars. Aldosterone secretion was always markedly elevated, and serum renin levels were abnormally low. Responses of aldosterone and renin to manipulations in sodium intake were blunted. Potassium repletion was more easily accomplished when dietary sodium was reduced.

From Ledingham et al.


Figure 40.

Renal–adrenal axis is hormonal cascade involving renin, angiotensin, and aldosterone for regulation of sodium and potassium balance and blood pressure. Interaction is depicted as it was first discovered in studies of patients with malignant hypertension in whom, because of defective feedback, it is involved in causation. Accordingly, there is massive excess of both renin and aldosterone that cannot turn itself off.

From Laragh et al.


Figure 41.

Different high blood pressure mechanisms, pathophysiological changes, and treatment strategies in high and low renin hypertensive patients.

Adapted from Laragh et al.


Figure 42.

Different blood pressure mechanisms in two animal models of renovascular (i.e., Goldblatt) hypertension. Although comparable blood pressure elevation occurs in Goldblatt hypertension of either the one‐kidney or two‐kidney type, different mechanisms are involved. Volume overexpansion from impaired renal excretory capacity is implicated in one‐kidney type, whereas renin‐initiated vasoconstriction appears largely responsible for two‐kidney type.

From Laragh et al.


Figure 43.

Dramatic difference in 60‐min plasma renin response to single oral dose of converting enzyme inhibitor captopril between patients with essential hypertension and those with renovascular disease. Response is used as basis of screening test for renovascular hypertension.

From Mueller et al.


Figure 44.

Renal angioplasty reduces plasma renin activity into normal range in patients with renovascular hypertension. Left: before angioplasty; right: 6 months after angioplasty. Hatched area shows normal range of plasma renin in relation to concurrent 24 h urine sodium excretion.

From Pickering et al.


Figure 45.

Renal vein renin diagnostic patterns. In essential hypertension (top), renin level in each renal vein is ∼25% greater than peripheral arterial, venous, or infrarenal inferior vena caval renin at all levels of renin secretion. In setting of unilateral renin secretion (curable renovascular hypertension; bottom left), affected kidney is solely responsible for maintaining peripheral renin levels. Hence, increment is at least 50% (0.5) and becomes progressively greater as renal blood flow is reduced. Patients with unilateral secretion of renin and normal BUN and'serum creatinine can usually be cured by angioplasty, surgical repair, or nephrectomy. But, if BUN and serum creatinine are elevated, bilateral disease is likely, even if contralateral suppression of renin secretion is observed. Unequal bilateral renin secretion (bottom right) indicates bilateral disease and decreases change of cure following unilateral nephrectomy, but improvement or even cure may be possible following angioplasty or corrective surgery. V1, renal vein renin; V2, renal vein renin on opposite side; IVC, inferior vena caval renin. Bold face large numbers indicate levels of plasma renin at the sites indicated.

From Laragh & Seale


Figure 46.

Relation of noon ambulatory plasma renin activity (left) and corresponding daily urinary aldosterone excretion (right) to concurrent daily rate of urinary sodium excretion. Dashed lines outline normal channel derived from study of normotensive people (see Fig. ). Total of 219 patients with untreated essential hypertension were studied, some on several occasions and at different levels of sodium intake. Three major subgroups (▴, low renin, ○, normal renin, and ▪, high renin essential hypertension) are defined by appropriateness or normalcy of plasma renin activity to rate of sodium excretion, used as index of dietary intake. Additional abnormal subgroups are defined when aldosterone (right) is included in the analysis.

From Brunner et al.


Figure 47.

Response to intravenous converting enzyme inhibition (MK 422) based on specific mechanisms of vasoconstriction. Left: High renin heart failure patient has prompt hemodynamic improvement following small dose of intravenous enalaprilat with further improvement in repeat challenge. Right: Low renin patient with comparable heart failure did not respond to intravenous enalaprilat but had prompt response to oral calcium channel inhibitor nifedipine (10 mg). Findings are representative of relative selectivity of response based on the mechanism of vasoconstriction. MAP, mean arterial pressure; PCWP, pulmonary capillary wedge pressure; CI, cardiac index; SVR, systemic vascular resistance.

From Cody et al.
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John H. Laragh, Jean E. Sealey. Renin–Angiotensin–Aldosterone System and the Renal Regulation of Sodium, Potassium, and Blood Pressure Homeostasis. Compr Physiol 2011, Supplement 25: Handbook of Physiology, Renal Physiology: 1409-1541. First published in print 1992. doi: 10.1002/cphy.cp080231