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

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.