Rgj. Westendorp et al., EFFECTS OF HYPOXIA AND ATRIAL-NATRIURETIC-PEPTIDE ON ALDOSTERONE SECRETION IN HEALTHY-SUBJECTS, Journal of applied physiology, 75(2), 1993, pp. 534-539
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.