Potassium stimulation of aldosterone secretion in vivo is reversed by nisoldipine, a calcium transport antagonist.
The effects of a novel calcium transport antagonist, nisoldipine, on K-stimulated aldosterone secretion have been examined in vivo. Direct KCl infusion into the adrenal gland stimulated aldosterone secretion. Infusion of nisoldipine, concomitantly with KCl at two rates, abolished the stimulation of aldosterone independently of its effects on K transport. The results suggest that K stimulation of aldosterone secretion in vivo is at least in part mediated by alterations in transmembrane Ca flux.
D000311:Adrenal Glands / Q000187:drug effects / Q000378:metabolism*; D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D005260:Female; D006854:Hydrocortisone / Q000378:metabolism; D007700:Kinetics; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015737:Nisoldipine; D011189:Potassium Chloride / Q000494:pharmacology*; D012756:Sheep
D002121:Calcium Channel Blockers; D000450:Aldosterone; D015737:Nisoldipine; D011189:Potassium Chloride; D009543:Nifedipine; D006854:Hydrocortisone