AJP - Endocrinology and Metabolism, Vol 254, Issue 5 E566-E571, Copyright © 1988 by American Physiological Society
Role of Ca2+ in response of aldosterone to stimulation by angiotensin II in vivo
E. I. Johnson, J. G. McDougall, J. P. Coghlan, D. A. Denton, B. A. Scoggins and R. D. Wright
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Victoria, Australia.
The role of Ca2+ in stimulation of aldosterone secretion (ASR) has been
evaluated in vivo using conscious sheep with an adrenal cervical
autotransplant. The calcium antagonists verapamil, nisoldipine, and
lanthanum and the calcium ionophore BAY K 8644 were infused into the
adrenal arterial supply before or concomitantly with angiotensin II.
Nisoldipine reversed stimulation of ASR (n = 4) from 13.6 +/- 3.2 to 4.8
+/- 1.2 nmol/h (P less than 0.01; control 2.3 +/- 0.6 nmol/h), as did
verapamil. Lanthanum had an intermediate effect. In contrast, pretreatment
with nisoldipine (n = 5) did not affect the response to angiotensin II,
with ASR being 3.8 +/- 0.9 nmol/h after nisoldipine alone and 12.8 +/- 1.3
nmol/h after nisoldipine plus angiotensin II. In response to graded
infusion of angiotensin II, nisoldipine blunted (P less than 0.01) to a
small degree the response at all doses of the peptide. Close adrenal
arterial infusion of the ionophore BAY K 8644 similarly reversed
stimulation of ASR by angiotensin II. It also blocked the initiation of
response to the peptide. These data are consistent with the involvement of
two pools of calcium in the zona glomerulosa response to angiotensin II, an
intracellular pool that is primarily responsible for the initiation of
response and a transmembrane extracellular pool that is primarily involved
in the "sustained" response to angiotensin II.
