AJP - Regulatory, Integrative and Comparative Physiology, Vol 256, Issue 5 1155-R1159, Copyright © 1989 by American Physiological Society

ARTICLES

Physiological doses of atrial peptide inhibit angiotensin II-stimulated aldosterone secretion

C. H. Metzler and D. J. Ramsay
Department of Physiology, University of California, School of Medicine, San Francisco 94143.

The current study was designed to investigate the potential of atrial peptide to serve as a physiological regulator of aldosterone secretion. Conscious chronically instrumented dogs were given a constant intravenous infusion of either atrial peptide [ANP-(1-28); 5, 25, or 100 ng.kg-1.min-1] or vehicle (saline). Once steady-state conditions were achieved, angiotensin II was infused in a ramp design to stimulate aldosterone secretion (2.5-40 ng.kg-1.min-1). In the absence of atrial peptide, angiotensin II induced dose-dependent increases in plasma aldosterone concentration. In the presence of a 5-ng.kg-1.min-1 infusion of atrial peptide, the aldosterone response was reduced an average of 65 +/- 11%. When atrial peptide was infused at 25 and 100 ng.kg-1.min-1, the response was totally abolished. These results show that atrial peptide is a potent inhibitor of angiotensin II-stimulated aldosterone secretion. The results suggest that normal variations in plasma atrial peptide concentration can play an important role in the regulation of aldosterone secretion and fluid and electrolyte balance.