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

• Published in: The American journal of physiology Vol. 256; no. 6 Pt 1; pp. E760 - E764
• Main Authors: Radke, K J, Clendenin, 3rd, R E, Taylor, Jr, R E, Schneider, E G
• Format: Journal Article
• Language: English
• Published: United States 01-06-1989
• Subjects: Adrenal Glands - drug effects; Adrenal Glands - secretion; Aldosterone - secretion; Angiotensin II - pharmacology; Animals; Calcium - pharmacology; Dogs; Female; Hypertonic Solutions; In Vitro Techniques; Kinetics; Male; Osmolar Concentration; Potassium - pharmacology
• ISSN: 0002-9513
• DOI: 10.1152/ajpendo.1989.256.6.E760

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.