Renal vascular response to interruption of the renin-angiotensin system in normal man

Hollenberg, Norman K.; Williams, Gordon H.; Taub, Ken; Ishikawa, Isao; Brown, Colin; Adams, Douglass F.

doi:10.1038/ki.1977.113

Cited by 80 publications

(37 citation statements)

References 30 publications

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“…An alternative hypothesis is that captopril lowers elevated intrarenal AII levels. AII is known to be generated in the kidney and arteriovenous All gradients have been demonstrated across it (20). Higher than normal intrarenal AII levels could make the juxtaglomerular AII receptor less responsive to infused AII (similar to reports of the glomerular AII receptor) (21) or these levels could exert a renal arteriolar vasoconstrictive effect, thereby providing a stimulus for continuous renin release.…”

Section: Discussionmentioning

confidence: 99%

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

et al. 1982

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A B S T R A C T The suppression of renin release by angiotensin II (All) (the so-called short feedback loop) is blunted in essential hypertension. To determine whether this abnormality is reversible, renin release was assessed in sodium-restricted essential hypertensives and normal controls: (a) during the administration of captopril for varying intervals and (b) following the infusion of graded doses of All (0.3-3 ng/kg per min) before and after plasma levels of AII had been chronically reduced with captopril (25-50 mg every 6 h) for 70 h.In control subjects, the maximal increment above control in plasma renin activity (PRA) after a single dose of captopril (11.9±3 ng/ml per h) was significantly (P < 0.02) greater than in hypertensives (8.1±1.7 ng/ml per h) despite similar reductions in AII levels and significantly greater decrements in diastolic blood pressure in the hypertensives. When captopril was continued for 70 h, the PRA increments above base line in hypertensive subjects (11.4±2.9 ng/ml per h) rose to levels seen in the controls (11±2.6 ng/ml per h); there were no significant differences in the AII or diastolic blood pressure decrements between the two groups.Compared with normotensive subjects, AII failed to suppress renin release in hypertensive subjects despite significantly greater diastolic blood increments and comparable All levels achieved at each All dose.After captopril treatment, All now produced significant declines in PRA in the hypertensives; moreover, comparing declines pre-and postcaptopril, This work was presented at the 63rd Annual Meeting of the Endocrine Society, Abstract 714, Cincinnati, OH.

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Section: Discussionmentioning

confidence: 99%

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

et al. 1982

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“…2) to a quantitatively similar extent, in normal subjects ingesting a sodium-restricted intake, sufficient to induce a documented activation of the renin-angiotensin system. 28 Moreover, the dose of converting enzyme inhibitor that induced a threshold increase in renal blood flow was the same as that which induced a sharp drop in plasma angiotensin II concentration; plasma bradykinin concentration was not modified. 2 * Taken in all, this evidence suggests that in normal man, as in the dog, the entire renal vascular response to a modest volume stimulus can be accounted for on the basis of a direct action of angiotensin II on renal blood supply.…”

mentioning

confidence: 80%

“…Saralasin and SQ 20,881 both failed to increase renal blood flow in normal subjects ingesting sodium and potassium sufficient to depress the reninangiotensin system. 28 Conversely, both classes of agent increased renal blood flow ( fig. 2) to a quantitatively similar extent, in normal subjects ingesting a sodium-restricted intake, sufficient to induce a documented activation of the renin-angiotensin system.…”

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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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“…10 RAS blockade was found to cause a marked increase in renal blood flow without affecting glomerular filtration rate. Consequently filtration fraction was reduced.…”

Section: The Pastmentioning

confidence: 99%

Blockade of the renin-angiotensin system for renal future perspectives protection: from history to future perspective

Burnier¹

2007

J Renin Angiotensin Aldosterone Syst

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Renal vascular response to interruption of the renin-angiotensin system in normal man

Cited by 80 publications

References 30 publications

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

Abnormal Renin Short Feedback Loop in Essential Hypertension Is Reversible with Converting Enzyme Inhibition

Converting enzyme inhibition and the kidney.

Blockade of the renin-angiotensin system for renal future perspectives protection: from history to future perspective

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