AJP - Endocrinology and Metabolism, Vol 248, Issue 6 676-E680, Copyright © 1985 by American Physiological Society
Ca antagonists do not alter aldosterone secretion during established Na depletion
E. I. Johnson, J. G. McDougall, J. P. Coghlan, D. A. Denton, K. J. Hardy, B. A. Scoggins and R. D. Wright
Conscious sheep whose sole adrenal gland had been transplanted to the neck
to allow access to the adrenal vasculature were used to study the effect of
calcium antagonists on aldosterone secretion. All animals were sodium
depleted by uncompensated loss of parotid saliva. The drugs EDTA,
verapamil, methoxyverapamil, nisoldipine, lanthanum,
propylmethylenedioxyindene, and ryanodine were infused on separate
occasions in three or four increasing dose levels. All infusions were made
to produce known concentrations directly into the adrenal arterial blood
supply. None of these infusions had any significant effect on aldosterone
secretion rate, cortisol secretion rate, and little or no effect on plasma
[Na], [K], or blood pressure. At high infusion rates some agents
(verapamil, methoxyverapamil) caused tachycardia. In contrast, angiotensin
II stimulation of aldosterone secretion is inhibited by both verapamil and
nisoldipine. The data demonstrate that the sustained elevation of
aldosterone secretion caused by sodium depletion is not dependent on a
sustained alteration in transmembrane calcium flux. Furthermore, if
circulating angiotensin II is the primary stimulus to aldosterone during
sodium depletion, its mechanism of action appears to switch to one which is
not dependent on calcium alone.
