AJP - Endocrinology and Metabolism, Vol 243, Issue 6 450-E457, Copyright © 1982 by American Physiological Society
Stimulation of aldosterone biosynthesis by sodium sequestration: role of angiotensin II
J. Muller, E. G. Lund, L. Hofstetter, D. B. Brunner and P. Haldy
The role of angiotensin II in the stimulation of aldosterone biosynthesis
by sodium sequestration in potassium-deficient rats was assessed by
experiments involving 1-day angiotensin II infusion, converting enzyme
inhibition, and bilateral nephrectomy. In intact rats, only an extremely
high dose of exogenous angiotensin II imitated the stimulatory effects of
polyethylene glycol-induced edema on the conversions of deoxycorticosterone
and corticosterone to 18-hydroxycorticosterone and aldosterone. Treatment
with the converting enzyme inhibitor captopril as well as bilateral
nephrectomy blocked the aldosterone-stimulating action of edema. This
inhibition was prevented by the simultaneous infusion of angiotensin II in
captopril-treated rats but not in nephrectomized animals. According to
these results, angiotensin II is an essential mediator in the stimulation
of aldosterone biosynthesis by sodium sequestration. However, the role of
the kidneys appears to be twofold. First, they act through the secretion of
renin. In addition, a second yet unknown kidney factor is necessary for a
full response of the zona glomerulosa to the stimulatory action of
angiotensin II.
