EFFECTS OF HYPOXIA AND ATRIAL-NATRIURETIC-PEPTIDE ON ALDOSTERONE SECRETION IN HEALTHY-SUBJECTS

To evaluate the inhibitory effect of hypoxia and atrial natriuretic pe ptide (ANP) on aldosterone secretion, 11 healthy male subjects were in fused with 5 ng . kg-1 . min-1 ANP or placebo. The subjects were expos ed in a stepwise fashion to incremental hypobaric hypoxia, which decre ased arterial oxygen saturation to 79 +/- 2% in the placebo and 84 +/- 2% in the ANP condition (P < 0.05). In the placebo condition, the pla sma ANP concentration increased from 13.8 +/- 1.0 to 19.6 +/- 2.3 pmol /l (P < 0.01) at the lowest barometric pressure. Plasma renin activity did not change, whereas the plasma aldosterone levels increased conse quent to the increase of plasma adrenocorticotropic hormone (ACTH). Co ntinuous infusion of ANP increased the plasma levels twofold (P < 0.00 1) and the level of guanosine 3,5'-cyclic monophosphate threefold (P < 0.001). However, the plasma aldosterone concentrations were not diffe rent in the two experimental conditions. Administration of supplementa ry oxygen significantly decreased ACTH to baseline values (P < 0.01) t ogether with a decrease in aldosterone. Free water clearance (P = 0.05 ) but not sodium excretion (P = NS) increased during continuous ANP in fusion. The data indicate that the aldosterone secretion in hypoxia is not inhibited by (patho)physiological plasma ANP levels. The inhibiti on of aldosterone secretion may well be explained by a direct effect o f hypoxia on the adrenal cells. ACTH is a major stimulus of aldosteron e secretion in hypoxia, which overrides the natriuretic effect of ANP.