Calcium dependence of osmolality-, potassium-, and angiotensin II-induced aldosterone secretion.

Different calcium-dependent mechanisms may be involved in mediating stimulus-induced aldosterone secretion. Using isolated perfused canine adrenal glands, we determined the effect of reductions in extracellular [Ca2+] and of infusion of a voltage-dependent calcium channel antagonist, nifedipine, on aldosterone secretion induced by decreases in osmolality, by increases in [K+], or by infusion of angiotensin II (ANG II). Aldosterone secretion was stimulated to a similar level by reducing osmolality, by increasing [K+], or by infusing ANG II. After 50 min of stimulation, lowering [Ca2+] from 1.25 to 0.10 mM caused a marked and similar inhibition of osmolality- and [K+]-induced aldosterone secretion that was significantly greater than inhibition of ANG II-induced aldosterone secretion. Similarly, nifedipine at 3.3 X 10(-8) M caused marked and similar inhibition of osmolality- and [K+]-induced aldosterone secretion that was significantly greater than the inhibition of ANG II-induced aldosterone secretion. These data demonstrate that calcium-dependent processes are involved in osmolality-, [K+]-, and ANG II-induced aldosterone secretion. However, the calcium-dependent process(es) evoked by reductions in osmolality or increases in [K+] are considerably different from that evoked by ANG II. Osmolality and potassium appear to induce aldosterone secretion primarily by activating voltage-dependent calcium channels.