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 Copyright Permission Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by BRALEY, L. M. Articles by WILLIAMS, G. H. Search for Related Content PubMed PubMed Citation Articles by BRALEY, L. M. Articles by WILLIAMS, G. H.

Sodium-Mediated Modulation of Aldosterone Secretion: Impact of Converting Enzyme Inhibition on Rat Glomerulosa Cell Response to Angiotensin-II^*

Endocrine-Hypertension Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School Boston, Massachusetts 02115

Address all correspondence and requests for reprints to: Gordon H. Williams, M.D., Endocrine-Hypertension Division, Brigham and Women's Hospital, 221 Longwood Avenue, Boston, Massachusetts 02115.

Abstract

Sodium restriction enhances the aldosterone response to angiotensin-II (All) in normal rats, but not in spontaneously hypertensive rats (SHR). To determine whether a change and/or abnormality in the circulating or adrenal reninangiotensin systems are responsible for these observations, three groups of animals were studied on a low sodium diet with and without the administration of a converting enzyme inhibitor (enalapril). Sprague-Dawley and Wistar-Kyoto (normotensive rat strains) and SHR were placed on low sodium (0.1%) for 9 days, the last 4 days of which enalapril was administered to half of the animals. In all groups enalapril treatment resulted in a significant (P < 0.001) reduction in blood pressure, an increase in renin activity, and a reduction in plasma aldosterone when all of the animals were considered together, although the change in blood pressure achieved statistical significance only in the Wistar-Kyoto rats. Additionally, basal aldosterone output from isolated glomerulosa cells was lower in the normotensive animals pretreated with enalapril. However, despite the evidence for inhibition of converting enzyme, there was no change in the hypertensive animals. Thus, neither locally nor systemically generated All appear to participate in the maintenance of the increased aldosterone responsiveness to All with sodium restriction. Furthermore, they do not appear to contribute to the altered adrenal responsiveness to All with sodium restriction in SHR. These data provide further support for the hypothesis that as yet undefined glomerulosa intracellular mechanisms are altered by dietary sodium restriction in normotensive, but not hypertensive, rats.

Footnotes

^* This work was supported by NIH SCOR Grant in Hypertension HL-36568 and Training Grant in Hypertension HL-07609.

Received February 17, 1989.

This article has been cited by other articles:

				B. Peters, P. Teubner, S. Clausmeyer, T. Puschner, C. Maser-Gluth, H.-J. Wrede, B. Kranzlin, and J. Peters StAR expression and the long-term aldosterone response to high-potassium diet in Wistar-Kyoto and spontaneously hypertensive rats Am J Physiol Endocrinol Metab, January 1, 2007; 292(1): E16 - E23. [Abstract] [Full Text] [PDF]

				J. S. Williams and G. H. Williams 50th Anniversary of Aldosterone J. Clin. Endocrinol. Metab., June 1, 2003; 88(6): 2364 - 2372. [Full Text] [PDF]