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

Abstract

Sodium restriction enhances the aldosterone response to angiotensin-II (AII) in normal rats, but not in spontaneously hypertensive rats (SHR). To determine whether a change and/or abnormality in the circulating or adrenal renin-angiotensin 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 less than 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 AII appear to participate in the maintenance of the increased aldosterone responsiveness to AII with sodium restriction. Furthermore, they do not appear to contribute to the altered adrenal responsiveness to AII 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.