AJP - Regulatory, Integrative and Comparative Physiology, Vol 253, Issue 6 832-R837, Copyright © 1987 by American Physiological Society
Angiotensin II sensitization of aldosterone responsiveness to plasma sodium in conscious dogs
D. C. Merrill, M. M. Skelton and A. W. Cowley Jr
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
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+.
