This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Rabinowe, S. L. Articles by Williams, G. H. Search for Related Content PubMed PubMed Citation Articles by Rabinowe, S. L. Articles by Williams, G. H.

Hypertension, Vol 10, 404-408, Copyright © 1987 by American Heart Association

ARTICLES

Renin suppression by saline is blunted in nonmodulating essential hypertension

SL Rabinowe, JE Redgrave, DM Shoback, S Podolsky, NK Hollenberg and GH Williams
Department of Medicine, Harvard Medical School, Boston, Massachusetts.

We have reported that 50% of subjects with normal renin essential hypertension have both delayed suppression of the renin-angiotensin- aldosterone axis following sodium infusion and a delayed rate of excretion of an acute salt load. In another study we have also described a subset of patients with essential hypertension (called nonmodulators) who have several abnormalities, including a pressor response to salt loading. To evaluate whether the abnormalities described in these different groups of patients actually occur in the same patient, we assessed the renin-angiotensin-aldosterone axis response to short-term saline loading in 38 hypertensive patients. Their ability to modulate was determined by their renal vascular response to infused angiotensin II on a high salt diet (200 mEq Na). In response to a 3-hour infusion of saline, 75 mEq/hr, the reduction in plasma renin activity at both 60 and 120 minutes was significantly greater (p less than 0.008) in patients with normal modulation than in the nonmodulators. Plasma aldosterone levels were also significantly lower (p less than 0.001) in those with intact modulation. Thus, nonmodulating essential hypertensive patients have abnormalities in several systems that influence sodium homeostasis, including altered adrenal and renal vascular response to angiotensin II, altered renal blood flow response to salt loading, and a delayed suppression of the renin-angiotensin-aldosterone system with short-term saline infusion.

This article has been cited by other articles:

				D. A. Price, N. D.L. Fisher, M. C. Lansang, R. Stevanovic, G. H. Williams, and N. K. Hollenberg Renal Perfusion in Blacks: Alterations Caused by Insuppressibility of Intrarenal Renin With Salt Hypertension, August 1, 2002; 40(2): 186 - 189. [Abstract] [Full Text] [PDF]

				P. van Paassen, D. de Zeeuw, G. Navis, and P. E. de Jong Does the Renin-Angiotensin System Determine the Renal and Systemic Hemodynamic Response to Sodium in Patients With Essential Hypertension? Hypertension, February 1, 1996; 27(2): 202 - 208. [Abstract] [Full Text]