A dynamic study of plasma renin activity and aldosterone concentration in normal and hypertensive subjects

Bayard, Françis; Alicandri, C; Beitins, Inese Z.; Lubash, Glenn D.; Kowarski, Avinoam; Migeon, Claude J.

doi:10.1016/0026-0495(71)90126-0

Cited by 18 publications

(7 citation statements)

References 10 publications

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“…Luetscher et al 16 reported that, when compared with normotensive subjects, patients with essential hypertension on a normal sodium intake showed normal responsiveness to renin but an enhanced plasma aldosterone response to upright posture. Similar findings were reported by Bayard et al, 17 who assessed the relative renin and aldosterone response to furosemide administration in normal controls and patients with essential hypertension on normal and high sodium intakes.…”

Section: Discussionsupporting

confidence: 76%

Enhanced aldosterone response to angiotensin II in human hypertension.

Kisch¹,

Dluhy²,

Williams³

1976

Circulation Research

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SUMMARY Adrenal and vascular responsiveness to graded doses of angiotensin II (A II) were recorded for seven normal subjects and 12 patients with essential hypertension while in balance on an intake of 200 mEq sodium/100 mEq potassium. Patients with essential hypertension had been previously studied and known to have normal responses of plasma renin activity to sodium restriction and upright posture. A l l was administered for 30 minutes at rates of 0.1, 0.3, 1, and 3 ng/kg per minute and plasma aldosterone responses were assessed 20 and 30 minutes later; blood pressure was monitored at intervals of 1 minute during infusion of A 11 at each rate. A significant increment in plasma aldosterone occurred at an infusion rate of 0.3 ng/kg per minute in patients with hypertension. This change was not seen until the infusion rate reached 1.0 ng/kg per minute in the normotensive control subjects. Even at an A II infusion rate of 1 ng/kg per minute, the increment in plasma aldosterone levels in normotensive subjects (4.2 ± 0.6 ng/dl) was significantly less (P < 0.001) than that in patients with essential hypertension (19 ± 3 ng/dl). In both groups, a significant rise in mean arterial blood pressure occurred at an A II dose of 0.3 ng/kg per minute, but the pressor response of the hypertensive group was significantly greater at the highest infusion rate (3 ng/kg per minute) (P < 0.05). Thus, enhanced adrenal and pressor responsiveness to infused A II was observed in the hypertensive subjects, suggesting a change in A II receptor affinity.ANGIOTENSIN II may play an important role in the control of blood pressure through its vasoconstrictor activity as well as its effects on volume homeostasis exerted through regulation of aldosterone secretion. However, previous studies evaluating adrenal and vascular responsiveness to infused angiotensin II (A II) in hypertensive subjects have yielded conflicting results.1 ' 6 Moreover, recent studies suggest that there may be physiologically important but functionally different receptors for A II on the adrenal cortex and vascular smooth muscle.7 ' 9 An imbalance of the relative responsivenes of these receptors to A II might lead to an imbalance in volume homeostasis or vasoconstrictor activity and thus produce an elevated blood pressure. The present study was designed to compare the relative magnitude of response of blood pressure and aldosterone secretion to graded doses of A II in patients with essential hypertension and normal subjects. MethodsTwelve patients with essential hypertension and seven normotensive control subjects were studied in the Clinical Research Center of the Peter Bent Brigham Hospital. The normotensive subjects (five male, two female) ranged in age from 23 to 38 years. They denied use of drugs and had no evidence of renal, cardiovascular, or endocrine abnormalities on routine screening. Patients with essential hypertension (eight male, four female) ranged in age from 24 to 68 years. The criteria for inclusion of patients with hyperten- sion in the study were as follo...

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Section: Discussionsupporting

confidence: 76%

Enhanced aldosterone response to angiotensin II in human hypertension.

Kisch¹,

Dluhy²,

Williams³

1976

Circulation Research

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“…This could explain the dissociation of the renin-angiotensin aldosterone axis during sodium loading (5-7), prolonged recumbency (8), and upright posture (4, 6) and after furosemide-induced sodium depletion, as observed in a patient reported by Bayard et al (18) and in the patients in this study. However, other explanations need to be considered.…”

Section: Discussionsupporting

confidence: 65%

Increased Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension

Wisgerhof¹

1978

J. Clin. Invest.

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A B S T R A C T Studies were undertaken to determine if the dissociation of aldosterone and plasma renin activity in low-renin essential hypertension is due to altered adrenal responsiveness to angiotensin II. The responsiveness of' the adrenal glands to angiotensin II was determined by infusing graded doses of angiotensin II into normal subjects and into patients with essential hypertension and measuring changes in levels of' plasma aldosterone in response to the infusion. To minimize the influence of endogenous angiotensin II and ACTH, supplemental sodium and dexamethasone were given before the infusions. Levels of plasma aldosterone and plasma renin activity were determined in normal subjects anid in the same patients after the combined stimuli of furosemide and upright posture, a maneuver used to increase the level of endogenous angiotensin II. To determine if the changes in levels of plasma aldosterone during infusion of angiotensin II were due to alteration of the metabolic clearance of aldosterone, the metabolic clearance of aldosterone was meastured before and during the infusion of angiotensin II.After sodium loading, dexamethasone treatment, and supine posture, levels of plasma aldosterone of normal subjects and patients with essential hypertension were suppressed equally. In response to the infusion of angiotensin II, the levels of plasma aldosterone of patients with low-renin essential hypertension were significantly higher than those of normal subjects or of patients with normal-renin essential hypertension.

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“…From the work on adults, in which renin and aldosterone responses to various stimuli have been studied, it might be anticipated that aldosterone responses to renin stimulation are delayed by 15 to 20 minutes (Bayard et al, 1971). We therefore felt that our findings reflected the shortness of the observation period.…”

Section: Resultsmentioning

confidence: 91%

Renin and aldosterone response in human newborns to acute change in blood volume.

Dillon¹,

Rajani²,

Shah³

et al. 1978

Archives of Disease in Childhood

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SUMMARY Increased activity of the renin/aldosterone system in the neonatal period is now well established in both animals and man but the control mechanisms are poorly understood. We have monitored the plasma renin activity (PRA) and plasma aldosterone concentration (PAldo) in 14 infants undergoing 21 exchange transfusions. PRA and PAldo were measured before and at 5, 10, 15, 30, 45, and 60 minutes after the injection, and 5, 10, 15, and 30 minutes after the withdrawal of 7 ml blood/kg birthweight immediately before exchange transfusions. PRA increased to a maximum of 53 % and decreased to a maximum of 39% of the resting values after withdrawal or injection of blood respectively. PAldo values did not change significantly during the same period. Thus the renin-angiotensin system in the newborn infant is responsive to changes in blood volume.

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A dynamic study of plasma renin activity and aldosterone concentration in normal and hypertensive subjects

Cited by 18 publications

References 10 publications

Enhanced aldosterone response to angiotensin II in human hypertension.

Enhanced aldosterone response to angiotensin II in human hypertension.

Increased Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension

Renin and aldosterone response in human newborns to acute change in blood volume.

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