Angiotensin II sensitization of aldosterone responsiveness to plasma sodium in conscious dogs.

Abstract

Studies were performed to quantify the interaction of angiotensin II (ANG II) and plasma sodium (Na+) on the adrenal gland's ability to secrete aldosterone (Aldo). Two groups of normal conscious dogs were used in which plasma Na+ was independently elevated in the face of differing background levels of ANG II. In group 1 (n = 6), plasma Na+ was increased progressively over a 1-h period (from 143 +/- 1 to 152 +/- 1.2 meq/l), whereas plasma K+ was maintained at a constant level by intravenous infusion. With low background levels of ANG II (0.5 ng.kg-1.min-1), plasma Aldo remained unchanged with the increase in plasma Na+. With high ANG II (20.0 ng.kg-1.min-1), plasma Na+ changed in a similar manner (143.1 +/- 1.2 to 154.3 +/- 0.7 meq/l), whereas plasma Aldo decreased progressively from 35.3 +/- 2.3 to 27.9 +/- 3.8 ng/dl (P less than 0.05). In group 2 (n = 5), plasma Na+ was increased abruptly (144.9 +/- 0.6 to 152.1 +/- 0.5) and maintained at the elevated level for 3 h, and plasma K+ was held constant. Again, at low steady-state levels of ANG II (0.5 ng.kg-1.min-1), plasma Aldo levels remained unchanged. But, at intermediate levels of ANG II (5.0 ng-kg-1.min-1), producing plasma ANG II levels similar to those seen with dietary NaCl restriction, plasma Aldo decreased from 20.4 +/- 4.3 to 9.0 +/- 1.3 ng/dl (P less than 0.05). This rate of infused ANG II has been shown to result in plasma ANG II levels similar to that seen with dietary NaCl restriction. At the highest dose of ANG II (20 ng.kg-1.min-1), the ability of plasma Na+ to lower plasma Aldo was blunted to the extent that the decrease from 27.5 +/- 2.2 to 21.3 +/- 1.6 was not statistically significant. These studies indicate that physiological elevation of ANG II appears to sensitize the adrenal aldosterone responsiveness to changes in plasma Na+.