Abnormal Responsiveness of the Renin Aldosterone System to Acute Stimulation in Patients with Essential Hypertension

Williams, Gordon H.; Rose, Leslie I.; Dluhy, Robert G.; Mccaughn, Donald; Jagger, Paul I.; Hickler, Roger B.; Lauler, David P.

doi:10.7326/0003-4819-72-3-317

Cited by 57 publications

(18 citation statements)

References 19 publications

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“…10 -11 Second, some hypertensive patients do not increase their aldosterone output in response to acute volume depletion in a manner similar to that observed in normotensive subjects. 12 Because the response of both the adrenal and the renal blood supplies with shifts in total body by guest on May 8, 2018 http://hyper.ahajournals.org/ sodium or effective blood volume is primarily determined by angiotensin II, the data suggested that the underlying difficulty was an abnormality in the interaction of these tissues with angiotensin II. Indeed, one study 13 suggested that these two defects were occurring in the same patient and that they might be related to an abnormality in the way the renal vasculature and adrenal sensitivity to angiotensin II change with sodium intake.…”

Section: Non-modulating Essential Hypertensionmentioning

confidence: 96%

Non-modulating hypertension. A subset of sodium-sensitive hypertension.

Williams

Hollenberg

1991

Hypertension

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Section: Non-modulating Essential Hypertensionmentioning

confidence: 96%

Non-modulating hypertension. A subset of sodium-sensitive hypertension.

Williams

Hollenberg

1991

Hypertension

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“…Recovery of added steroid from each assay is the same, ranging from 85 to 110%. The cortisol, corticosterone, and aldosterone values in 12 samples were compared with a double isotope derivative method previously used (8) which produced a correlation coefficient of 0.99 with a P value of correlation < 0.001 for all three steroids.…”

Section: Laboratory Proceduresmentioning

confidence: 99%

“…PRA was measured by a modification of the Boucher method as previously described (12 (13), utilizing a General Electric 635 computer. The results are expressed as mean ± standard error of the mean, and significance as P <0.02 unless otherwise indicated.…”

Section: Laboratory Proceduresmentioning

confidence: 99%

Studies of the Control of Plasma Aldosterone Concentration in Normal Man

Williams¹,

Tuck²,

Rose³

et al. 1972

J. Clin. Invest.

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A B S T R A C T The peripheral plasmna levels of aldosterone, renin activity, potassium, sodium, corticosterone, and cortisol were measured in six normal subjects four times daily-10 a.m., 2 p.m., 5 p.m., 11 p.m.-on 3 consecutive days. A constant daytime activity program was maintained throughout the study. After 5 days on a 10 mEq sodium/100 mEq potassium isocaloric intake, the mean upright 10 a.m. plasma renin activity was 1773±186 ng/100 xnl per 3 hr and the mean plasma aldosterone, 81±+14 ng/100 ml. These two parameters fell continuously throughout the day parallel to the fall in plasma cortisol and corticosterone. In response to 2 liters of normal saline infused from 10 a.m. to 2 p.m. on 2 consecutive days, plasma aldosterone levels fell significantly to 13±5 ng/100 ml at 2 p.m. after the 1st day's infusion and to 6±1 ng/100 ml at 2 p.m. after the 2nd. Plasma renin activity demonstrated a parallel fall to 368±63 ng/ 100 ml per 3 hr and 189±27 ng/100 ml per 3 hr at 2 p.m. on the 1st and 2nd days, respectively. There was no significant alteration in plasma levels of cortisol, corticosterone, potassium, or sodium on the 2 days of sodium loading in comparison with the control day. In an additional study, five normal supine subjects received 500 ml saline/hr for 6 hr. As in the 2 day study, plasma aldosterone and renin activity had parallel decrements at 1, 2, 4, and 6 hr after the start of the saline infusion. From these studies, it is concluded that plasma renin activity is the dominant factor controlling plasma aldosterone when sodium-depleted normal subjects are acutely repleted.Dr. Williams is an Investigator of the Howard Hughes Medical Institute.

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“…Streeten et al (21) were the first to report this alteration, noting that half their patients with normal renin essential hypertension had subnormal secretory responses to chronic volume depletion (sodium restriction). Since their studies, a dissociation between renin and aldosterone response to acute volume depletion (either venous hemorrhage or diuretic-induced) (3,(22)(23)(24) and a decreased adrenal response to infused A 11 (4) have also been reported. On the other hand, Kisch et al (1) and Wisgerhof and Brown (2) have suggested that some essential hypertensive patients, particularly those with low plasma renin levels, may have an increased adrenal responsiveness to A II.…”

Section: Resultsmentioning

confidence: 99%

“…A probit transformation defined the dose required to induce a 50% increase in aldosterone (ED50). In the patients in whom aldosterone rose with saralasin, the dose required to induce INTRODUCTION Recent studies have reported that adrenal responsiveness to angiotensin II (A II)I is altered (either increased [1,2] or decreased [3,4]) in some patients with essential hypertension. One possible explanation would be a functional change in the relative importance ofA II in the control ofaldosterone secretion or a change in the activity of a postreceptor event.…”

mentioning

confidence: 99%

The Adrenal Receptor for Angiotensin II is Altered in Essential Hypertension

Williams¹,

Hollenberg²,

Moore³

et al. 1979

J. Clin. Invest.

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A B S T R A C T To determine the mechanism underlying altered adrenal responsiveness in patients with essential hypertension, the renin-angiotensin-aldosterone axis was assessed in normotensive and hypertensive subjects using three pharmacological probes: SQ 20881, a converting enzyme inhibitor; saralasin, a competitive angiotensin antagonist with prominent agonist properties; and angiotensin itself. All subjects were studied while supine and in balance on a 10 meq Na/100 meq K intake. The decrement in plasma aldosterone with SQ 20881 in 26 hypertensive subjects (15+3 ng/dl) was normal (13±4 ng/dl), suggesting that the altered adrenal responsiveness in hypertensives is not because of a change in a postreceptor event or in the relative contribution of angiotensin to the control of aldosterone secretion.Saralasin at a dose (0.1 pug/kg per min) that reduced aldosterone levels in all normals produced a normal aldosterone decrement (14+±3 ng/dl) in 19 patients with renovascular hypertension (12±4 ng/dl). The same dose, however, had no net effect on plasma aldosterone levels in 70 patients with normal or high renin essential hypertension (-1±1 ng/dl) despite identical metabolic balance 3nd control renin and angiotensin levels. The altered response could be explained by an agonist effect, aldosterone rising in 45 of the essential hypertensives. There were no significant differences between normal and abnormal responders in pre-and postcortisol, -potassium, -renin and -angiotensin concentrations.Angiotensin was infused (0.1-3 ng/kg per min) in 15 patients with normal renin essential hypertension, previously studied with saralasin. A probit transformation defined the dose required to induce a 50% increase in aldosterone (ED50). In the patients in whom aldosterone rose with saralasin, the dose required to induce

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Abnormal Responsiveness of the Renin Aldosterone System to Acute Stimulation in Patients with Essential Hypertension

Cited by 57 publications

References 19 publications

Non-modulating hypertension. A subset of sodium-sensitive hypertension.

Non-modulating hypertension. A subset of sodium-sensitive hypertension.

Studies of the Control of Plasma Aldosterone Concentration in Normal Man

The Adrenal Receptor for Angiotensin II is Altered in Essential Hypertension

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