Calcium antagonists and stimulus-secretion coupling of aldosterone.
Sheep whose left adrenal gland had been autotransplanted to a combined carotid artery-jugular vein skin loop in the neck were used to study the role of calcium in stimulus-secretion coupling for aldosterone biosynthesis. The calcium antagonists nisoldipine and verapamil were infused directly into the adrenal arterial blood supply during Na depletion or in Na replete sheep during concomitant adrenal arterial infusion of angiotensin II or KC1. The stimulation of aldosterone secretion following angiotensin II (1 nmol/l blood flow) or KC1 (delta [K] 1 mmol/l blood flow) was totally blocked by both verapamil (10(-4) mol/l blood flow) and nisoldipine (2.6 X 10(-6) mol/l blood flow). In contrast, neither antagonist had any significant effect on the established hypersecretion of aldosterone caused by 24 h Na depletion as a result of parotid salivary loss. The data suggest an important role for calcium in stimulus-secretion coupling during acute stimulation by K and angiotensin II, but not in the longer-term sodium depletion. The data further suggest that angiotensin may not be the sole sustaining stimulus to aldosterone in sodium depletion or its mechanism switches from a Ca-dependent to a Ca-independent mechanism with Na depletion.
D000311:Adrenal Glands / Q000637:transplantation; D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D009543:Nifedipine / Q000031:analogs & derivatives / Q000494:pharmacology; D015737:Nisoldipine; D011188:Potassium / Q000502:physiology; D012756:Sheep; D012964:Sodium / Q000172:deficiency; D014182:Transplantation, Autologous; D014700:Verapamil / Q000494:pharmacology
D002121:Calcium Channel Blockers; D000804:Angiotensin II; D000450:Aldosterone; D015737:Nisoldipine; D012964:Sodium; D014700:Verapamil; D009543:Nifedipine; D011188:Potassium; D002118:Calcium