Renin, Angiotensin and Aldosterone in Human Pregnancy and the Menstrual Cycle

1971 ◽  
Vol 16 (3) ◽  
pp. 183-196 ◽  
Author(s):  
J. I. S. Robertson ◽  
R. J. Weir ◽  
G. O. Düsterdieck ◽  
R. Fraser ◽  
M. Tree
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin ◽  
Normal Pregnancy ◽  
Maternal Plasma ◽  
Plasma Aldosterone ◽  
Sodium Depletion ◽  
Aldosterone Secretion ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
In Pregnancy

Aldosterone secretion is frequently, although not invariably, increased above the normal non-pregnant range in normal pregnancy. Substantial increases in plasma aldosterone concentration have also been demonstrated as early as the sixteenth week. In pregnancy, aldosterone secretion rate responds in the usual way to changes in sodium intake. Plasma renin concentration is frequently, but not invariably, raised above the normal non-pregnant range. Plasma renin-substrate is consistently raised in pregnancy. Plasma angiotensin II has also been shown usually to be raised in a series of pregnant women. A significant positive correlation has been shown between the maternal plasma aldosterone concentration and the product of the concurrent plasma renin and renin-substrate concentrations. This suggests that the increased plasma aldosterone in pregnancy is the consequence of an increase in circulating angiotensin II, which in turn is related to the level of both renin and its substrate in maternal blood. For these reasons, estimations of renin activity in pregnancy are of dubious value. The increased renin, angiotensin and aldosterone concentrations may represent a tendency to maternal sodium depletion, probably mainly a consequence of the increased glomerular filtration rate. It is possible that the nausea and other symptoms of early pregnancy may be a consequence of this tendency to sodium depletion, with its attendant hormonal changes. In ‘pre-eclampsia’, renin and aldosterone values are generally slightly lower than in normal pregnancy. Human chorion can apparently synthesize renin independently of the kidney. The physiological significance of this remains at present obscure, but it seems unlikely that this source contributes much, if at all, to the often elevated maternal plasma renin. Plasma renin, renin-activity and angiotensin II concentrations, and aldosterone secretion are increased in the luteal phase of the menstrual cycle.

The Effect of Prostaglandin E2 Upon the Biochemical Response to Infused Angiotensin II in Human Pregnancy

1984 ◽  
Vol 66 (4) ◽  
pp. 399-406 ◽  
Author(s):  
F. Broughton Pipkin ◽  
J. C. Hunter ◽  
S. R. Turner ◽  
P. M. S. O'Brien
Keyword(s):  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Plasma Concentrations ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Pressor Effect ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Plasma Renin Concentration ◽  
Pressure Plasma

1. The effects of angiotensin II infusion without and with simultaneous infusion of prostaglandin E2 were studied in 25 women in second trimester pregnancy. Twenty received one infusion of angiotensin II alone, followed by its infusion simultaneously with prostaglandin E2; five received two identical infusions of angiotensin II alone as controls. 2. Angiotensin II infusion alone was associated with suppression of plasma renin concentration to levels inversely proportional to the evoked change in diastolic blood pressure. Plasma renin substrate concentration was unchanged, but plasma aldosterone concentration rose markedly. This rise was inversely proportional to the threshold for pressor effect of angiotensin II. 3. Prostaglandin E2 administration alone was associated with increased plasma renin concentrations. 4. The pressor effect of angiotensin II was blunted when given together with prostaglandin E2 and plasma concentrations of angiotensin II reached were lower. 5. Plasma renin concentration was again suppressed during the joint infusion regimen; the degree of suppression was inversely proportional to the change in diastolic pressure. Plasma aldosterone concentration rose, but did not differ in the control and experimental groups. 6. Thus although the renin-angiotensin system is stimulated in normal pregnancy, the normal control mechanisms are still functional, and the capacity for further increases in activity exists.

Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Competitive Inhibitor ◽  
Urinary Flow ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Renin Inhibition

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.

scholarly journals Effects of Ramipril on the Aldosterone/Renin Ratio and the Aldosterone/Angiotensin II Ratio in Patients With Primary Aldosteronism

Hypertension ◽  
2020 ◽  
Vol 76 (2) ◽  
pp. 488-496 ◽  
Author(s):  
Zeng Guo ◽  
Marko Poglitsch ◽  
Diane Cowley ◽  
Oliver Domenig ◽  
Brett C. McWhinney ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Ace Inhibitors ◽  
Primary Aldosteronism ◽  
Characteristic Curve ◽  
False Negative ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Plasma Aldosterone Concentration

The aldosterone/renin ratio (ARR) is currently considered the most reliable approach for case detection of primary aldosteronism (PA). ACE (Angiotensin-converting enzyme) inhibitors are known to raise renin and lower aldosterone levels, thereby causing false-negative ARR results. Because ACE inhibitors lower angiotensin II levels, we hypothesized that the aldosterone/equilibrium angiotensin II (eqAngII) ratio (AA2R) would remain elevated in PA. Receiver operating characteristic curve analysis involving 60 patients with PA and 40 patients without PA revealed that the AA2R was not inferior to the ARR in screening for PA. When using liquid chromatography-tandem mass spectrometry to measure plasma aldosterone concentration, the predicted optimal AA2R cutoff for PA screening was 8.3 (pmol/L)/(pmol/L). We then compared the diagnostic performance of the AA2R with the ARR among 25 patients with PA administered ramipril (5 mg/day) for 2 weeks. Compared with basally, plasma levels of equilibrium angiotensin I (eqAngI) and direct renin concentration increased significantly ( P <0.01 or P <0.05) after ramipril treatment, whereas eqAngII and ACE activity (eqAngII/eqAngI) decreased significantly ( P <0.01). The changes of plasma renin activity and plasma aldosterone concentration in the current study were not significant. On day 14, 4 patients displayed false-negative results using ARR_direct renin concentration (plasma aldosterone concentration/direct renin concentration), 3 of whom also showed false-negative ARR_plasma renin activity (plasma aldosterone concentration/plasma renin activity). On day 15, 2 patients still demonstrated false-negative ARR_plasma renin activity, one of whom also showed a false-negative ARR_direct renin concentration. No false-negative AA2R results were observed on either day 14 or 15. In conclusion, compared with ARR which can be affected by ACE inhibitors causing false-negative screening results, the AA2R seems to be superior in detecting PA among subjects receiving ACE inhibitors.

Longitudinal study of platelet angiotensin II binding in human pregnancy

1992 ◽  
Vol 82 (4) ◽  
pp. 377-381 ◽  
Author(s):  
Philip N. Baker ◽  
Fiona Broughton Pipkin ◽  
E. Malcolm Symonds
Keyword(s):  
Longitudinal Study ◽  
Angiotensin Ii ◽  
Post Partum ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Substrate ◽  
Plasma Renin Concentration ◽  
Plasma Angiotensin ◽  
In Pregnancy

1. Platelet angiotensin II binding, circulating angiotensin II levels, plasma renin substrate and plasma renin concentration were measured in a longitudinal study of 30 women during pregnancy and the puerperium. 2. There was a significant fall in platelet angiotensin II binding from 11 weeks gestation to 18 weeks gestation (P < 0.01). There were no further significant changes in platelet angiotensin II binding until after delivery, a significant rise in platelet angiotensin II binding being found at 6 weeks post partum as compared with at 36 weeks gestation (P < 0.01). There was no further significant change from 6 to 12 weeks post partum, and platelet angiotensin II binding at 6 and 12 weeks post partum in the pregnant cohort approximated to that in non-pregnant women. These changes parallel those known to occur in pressor responsiveness to angiotensin II in pregnancy. 3. Plasma angiotensin II concentration, plasma renin substrate and plasma renin concentration were all significantly higher during pregnancy than in the puerperium (P < 0.001). There were no significant changes during pregnancy in plasma angiotensin II concentration or plasma renin concentration, although plasma renin substrate rose throughout. 4. Significant inverse correlations between platelet angiotensin II binding and plasma angiotensin II concentration (P < 0.01), plasma renin substrate (P < 0.01) and plasma renin concentration (P 0>001) were found during pregnancy. These data suggest that down-regulation of platelet angiotensin II binding by the components of the renin-angiotensin system pertains in pregnancy. 5. We are currently investigating parallelism between platelet and vascular angiotensin-binding sites. If such is confirmed, studies of platelet angiotensin II binding in pregnancy may be of both basic physiological and clinical interest in relation to the hypertensive diseases of pregnancy.

Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats

1987 ◽  
Vol 72 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lynn Chartier ◽  
Ernesto L. Schiffrin
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Plasma Renin Activity ◽  
Natriuretic Peptide ◽  
Adrenocorticotropic Hormone ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Aldosterone Secretion ◽  
Atrial Natriuretic

1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. 3. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin–angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.

Effects of angiotensin II, ACTH, and KCl on the adrenal renin-angiotensin system in the rat

1990 ◽  
Vol 122 (3) ◽  
pp. 369-373 ◽  
Author(s):  
Hiroyuki Sasamura ◽  
Hiromichi Suzuki ◽  
Ryuichi Kato ◽  
Takao Saruta
Keyword(s):  
Angiotensin Ii ◽  
Statistical Significance ◽  
Renin Angiotensin System ◽  
Plasma Aldosterone ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Captopril Treatment

Abstract Angiotensin II, ACTH and potassium chloride were administered to rats for 6 days and the effects on adrenal renin-like activity and adrenal angiotensin II/III immunoreactivity were investigated. Rats infused with angiotensin II(140 pmol/min) either ip or sc showed increases in adrenal angiotensin II/III immunoreactivity (p<0.05) and plasma aldosterone concentration (p<0.05), but no change in adrenal renin-like activity. Captopril treatment of angiotensin Il-infused rats caused a slight decrease in angiotensin II/III immunoreactivity which did not reach statistical significance. In contrast, rats treated with ACTH (Cortrosyn-Z, 3 IU/day, sc) showed an increase in adrenal renin-like activity (p<0.01), but no significant change in adrenal angiotensin II/III immunoreactivity. Rats treated with KCl in drinking water showed increases (p<0.05) in adrenal renin-like activity, adrenal angiotensin II/III immunoreactivity, and plasma aldosterone. These results suggest that angiotensin II, ACTH and potassium, three major regulators of aldosterone secretion by the adrenal gland, have different effects on the adrenal renin-angiotensin system when administered in vivo.

EFFECT OF TWO CONSECUTIVE ACUTE STIMULI ON PLASMA ALDOSTERONE

1972 ◽  
Vol 71 (1) ◽  
pp. 153-159 ◽  
Author(s):  
Fred H. Katz ◽  
Peggy Romfh ◽  
Judith A. Smith
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Adrenal Cortex ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Upright Posture ◽  
Aldosterone Secretion ◽  
Stimulation Of

ABSTRACT The increase in plasma aldosterone and reduction in plasma renin activity induced by 30 to 60 minutes of mildly pressor angiotensin II infusion in man can be largely abolished when recent prior stimulation of the adrenal cortex by upright posture has been applied. A similar prevention of the ACTH-induced increase in plasma aldosterone can be achieved by previous upright ambulation. These results indicate the intermittent refractoriness of aldosterone secretion and that care must be exerted in the timing of any tests of aldosterone stimulation.

Modulation of aldosterone secretion in frusemide-induced hypokalaemia

1984 ◽  
Vol 107 (1) ◽  
pp. 91-96 ◽  
Author(s):  
Masaki Fujimaki ◽  
Shusaku Nagahama ◽  
Hiroko Suzuki ◽  
Ikuo Saito ◽  
Takao Saruta
Keyword(s):  
Angiotensin Ii ◽  
Adrenal Gland ◽  
Potassium Chloride ◽  
Serum Potassium ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Initial Increase ◽  
Aldosterone Secretion ◽  
Potassium Supplementation ◽  
Secretory Capacity

Abstract. To study the effect of hypokalaemia in the regulation of aldosterone secretion, repeated injections of frusemide (3 mg/kg) plus saline with or without simultaneous infusion of potassium chloride (1 mEq/kg/h) were performed in 24 conscious female rabbits for 7 h. Without potassium supplementation, the plasma renin activity (PRA) remained elevated throughout the study, while an initial increase (1 h to 3 h) in plasma aldosterone (PA) gradually returned to normal with reduction of the serum potassium. In rabbits on potassium supplements to prevent the development of hypokalaemia, both PRA and PA remained elevated. The incremental aldosterone response to administration of potassium chloride, angiotensin II or ACTH, was considerably smaller in potassium-depleted rabbits than in potassium-repleted rabbits. These results suggest that serum potassium modulates the effects of angiotensin II or ACTH on aldosterone secretion, and that a certain level of potassium is necessary to maintain the aldosterone secretory capacity of the adrenal gland.

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