AJP - Cell Physiology, Vol 256, Issue 1 C89-C95, Copyright © 1989 by American Physiological Society
Effect of ANP on sustained aldosterone secretion stimulated by angiotensin II
C. M. Isales, W. B. Bollag, L. C. Kiernan and P. Q. Barrett
Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06510.
The sustained aldosterone secretory response to angiotensin II (ANG II)
depends on receptor-mediated increases in membrane diglyceride (DG) and an
increase in calcium influx rate. These signals serve to activate
membrane-associated protein kinase C (PKC) and result in enhanced
phosphorylation of a unique set of proteins. These events can be mimicked
by the addition of a phorbol ester, 12-O-tetra decanoyl phorbol 13-acetate
(TPA), and a calcium ionophore, A23187, that bypass the initial
receptor-associated events. We studied the inhibitory action of atrial
natriuretic peptide (4-28 hANP) on the sustained secretory response to ANG
II in isolated bovine adrenal glomerulosa cells. Although 10 nM ANP
inhibited aldosterone secretion, it did not significantly alter the ANG
II-elicited rise in 45Ca2+ influx rate [control (CON): 0.44 +/- 0.06; ANG
II: 1.11 +/- 0.12 (P less than 0.001); ANG II + ANP: 1.18 +/- 0.14], the
steady-state level of aequorin luminescence [intracellular [Ca2+]
([Ca2+]i)], or the rise in cellular DG content [CON: 0.132 +/- 0.01; ANG
II: 0.194 +/- 0.01 (P less than 0.005); ANG II + ANP: 0.202 +/- 0.01
nmol/10(6) cells]. IN addition, ANP was able to inhibit aldosterone
secretion stimulated by the combined addition of A23187 + TPA. When protein
phosphorylation in the ANP-inhibited cells was evaluated, ANG II-induced
protein phosphorylation events were preserved. In contrast to the effect of
ANP, the calcium channel blocker nitrendipine abolished the ANG II-induced
rise in 45Ca2+ influx rate, reduced the steady-state level of [Ca2+]i, and
returned the phosphoproteins to their control states.(ABSTRACT TRUNCATED AT
250 WORDS)
