Reciprocal Influence of Salt Intake on Adrenal Glomerulosa and Renal Vascular Responses to Angiotensin II in Normal Man

Hollenberg, Norman K.; Chenitz, W; Adams, Douglass F.; Williams, Gordon H.

doi:10.1172/jci107748

Cited by 326 publications

(167 citation statements)

References 30 publications

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“…Acutely, angiotensin II (Ang II) affects the renal and peripheral vasculature and adrenal glomerulosa by reducing renal blood flow, enhancing vascular tone, and increasing aldosterone secretion. 1,2 All of these physiologic changes promote renal sodium conservation and maintenance of blood pressure.…”

Section: Introductionmentioning

confidence: 99%

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Altered sodium perception in essential hypertensive patients following rapid volume expansion

Conlin

Williams

et al. 1999

J Hum Hypertens

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We investigated sodium and volume-dependent mechanisms in the modulation of adrenal and renal vascular responsiveness to angiotensin II in hypertensive (n = 9) and normal subjects (n ‫؍‬ 5) who demonstrated normal responses during steady-state salt balance (intact modulation). Adrenal and renal vascular responses to angiotensin II were assessed on four occasions. These studies were performed during steady-state high salt and low salt balance and later during non-steady state conditions, after acute volume expansion with normal saline or dextran infusions. The volume expansion studies were administered while study subjects were in low salt balance. In both the normal and hypertensive patients saline and dextran suppressed plasma renin activity and aldosterone release, induced renal vasodilation and enhanced the renal vascular response to angiotensin II, similar to that observed during high salt

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Section: Introductionmentioning

confidence: 99%

“…2 However, most studies investigating control of the renin-angiotensinaldosterone system have been conducted during balanced, constant dietary salt intake. Free-living individuals often vary salt intake quite markedly balance.…”

Section: Introductionmentioning

confidence: 99%

Altered sodium perception in essential hypertensive patients following rapid volume expansion

Conlin

Williams

et al. 1999

J Hum Hypertens

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“…A similar relationship between renin level and sustained pressor response has been demonstrated during saralasin infusion. "2 Presumably, in low renin patients more vascular receptors are unoccupied by circulating angiotensin than in normal and high renin states, so that the partial agonistic effect of a given dose of saralasin will be greater and last longer9' [26][27][28][29][30][31][32] ( figs. 2 and 3).…”

Section: Discussionmentioning

confidence: 99%

Pressor response to saralasin (1-sar-8-ala-angiotensin II) bolus injection in hypertensive patients.

Waks¹,

Maxwell²,

Marks³

et al. 1978

Circulation

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SUMMARY A 10 mg bolus of the angiotensin blocker saralasin was injected 113 times in 68 subjects with essential or renovascular hypertension. Ninety percent of injections caused a transient increase in blood pressure, which correlated with plasma renin activity (PRA) (r = -0.54). Mean increase at 2 minutes was 21/13.4 mm Hg (P < 0.001) and was independent of pre-injection control blood pressure, with a rapid decrease to or below control values thereafter.Thirty-seven subjects were studied on successive days before and after furosemide-induced sodium depletion (152 ± 26 mEq [SE] A VASODEPRESSOR RESPONSE to intravenous administration of saralasin (1-sar-8-ala-angiotensin II), a competitive inhibitor of angiotensin II, signifies the presence of renin-mediated hypertension.1-7 We and others have suggested the use of saralasin testing in widespread screening of hypertensive patients.'I Because the usual method of saralasin administration, i.e., continuous, pump-controlled intravenous infusion, is not applicable for outpatient screening of large populations, we studied the effects of a single, rapid bolus injection of the drug." 8 We noted a close correlation of blood pressure responses to a bolus injection as compared to infusion of saralasin in patients with essential and renovascular hypertension, and concluded that the saralasin bolus test has many characteristics of an ideal screening procedure for renin-mediated hypertension.Severe pressor responses following saralasin infusions have been recently reported.9-12 However, there are few data concerning pressor responses to saralasin bolus administration.' Since the bolus technique involves rapid delivery of a relatively large quantity of saralasin to the receptor sites as compared to the various infusion techniques described,9 12 it has been predicted that saralasin bolus testing ". . . will sooner or later, result in a vascular catastrophe".' Accordingly, the present report presents a detailed systematic analysis of the pressor responses to 113 bolus injections in 68 hypertensive patients. Methods SubjectsThe study group consisted of 68 hypertensive patients (44 males and 24 females) who ranged in age from 10 to 62 years (mean age 40.1 years). Sixty-four were Caucasian and four were black. Before entry into the study, all patients were From sodium loss). In the low renin group, sodium depletion did not change PRA or the magnitude of the pressor response to saralasin, but significantly decreased control MAP by 13 mm Hg (P < 0.01). In normal and high renin patients, MAP was unchanged after diuresis, but PRA increased significantly and the pressor response was attenuated. The net effect of sodium depletion was to reduce the pressor response to saralasin in all renin subgroups by 9 to 12 mm Hg.Saralasin bolus injection, unlike infusion, saturates available vascular receptors only briefly, eliminating prolonged pressor responses.taken off antihypertensive medication for two weeks and then subjected to an extensive inpatient work-up designed to diagnose secondary f...

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“…In addition, as renal blood flow fell, the renal vascular response to angiotensin II was also reduced. 12 Circumstantial evidence, which raised the interesting possibility that the renal response was due to the direct action of angiotensin on the renal blood supply, was quickly tested in a number of species when pharmacologic antagonists became available. Many studies have documented an increase in renal blood flow in the dog and the rabbit when either class of agent is employed, 1 '"" but the interpretation of the functional response to the pharmacologic agents was complicated by the drop in arterial blood pressure when these agents were administered to animals in balance on a low salt diet.…”

Section: Renal Response To Pharmacologic Interruption In the Normal Smentioning

confidence: 99%

Converting enzyme inhibition and the kidney.

Meggs¹,

Hollenberg²

1980

Hypertension

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SUMMARY We review information on the renal response to converting enzyme inhibition, and attempt to evaluate the evidence that a reduction in angiotensin II formation is responsible for the renal response. There is little response to converting enzyme inhibitors in animals or man when the renln-angk>tensin system is suppressed by a literal sodium intake. With restriction of sodium intake, an increase in renal blood flow occurs; because a quantitatively similar response occurs to the angiotensin II analogs it is likely that the response reflects reversal of the local action of angiotensin II. In other settings it is not yet dear whether the renal response to converting enzyme inhibitor reflects only a reduction in angiotensin II formation or an additional action such as potentiation of the local actions of bradykinin or enhanced prostaglandin formation. Because these agents induce a potentiated increase in renal blood flow in the patient with essential hypertension, and with it an increase in glomerular filtration rate and sodium excretion in some patients, despite a fall in arterial pressure these questions have considerable importance. suggested that angiotensin, in addition to its systemic effect on blood pressure (BP) and on sodium homeostasis through control of aldosterone secretion, may have a direct action on the renal blood supply. 18 The important conceptual role played by ablation in defining the action of a hormone in an effector system was pointed out by Haber. 4 In the special case of the interaction of the renin-angiotensin system and the kidney, the kidney is both the source of the hormone and the responding organ. The ablation experiment, therefore, has clearly been impossible. For that reason, the development of several classes of agent that have made it possible to interrupt the renin-angiotensin system pharmacologically has made a major contribution to the evolution of our ideas.Before we convert pharmacologic responses to a physiologic interpretation, it is important that we assess the specificity of the available agents. The two

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Reciprocal Influence of Salt Intake on Adrenal Glomerulosa and Renal Vascular Responses to Angiotensin II in Normal Man

Cited by 326 publications

References 30 publications

Altered sodium perception in essential hypertensive patients following rapid volume expansion

Altered sodium perception in essential hypertensive patients following rapid volume expansion

Pressor response to saralasin (1-sar-8-ala-angiotensin II) bolus injection in hypertensive patients.

Converting enzyme inhibition and the kidney.

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