Intracellular mediators of potassium-induced aldosterone secretion.
We have investigated the intracellular messengers of potassium in eliciting aldosterone secretion in calf adrenal glomerulosa cells since there were unresolved issues relating to the role of phosphoinositides, cAMP and protein kinases. We observed no evidence of hydrolysis of phosphatidylinositol 4,5-bisphosphate (PIP2) in 3H-inositol labeled alf adrenal cells or increase of cAMP in response to potassium. Addition of calcium channel blocker, nitrendipine after stimulating adrenal glomerulosa cells with potassium, markedly inhibited aldosterone secretion. A calmodulin inhibitor (W-7) produced greater reduction of aldosterone secretion than an inhibitor of protein kinase C (H-7). These results suggest that a rise in cytosolic free calcium concentration through voltage-dependent calcium channel and calmodulin are the critical determinants of aldosterone secretion stimulated by potassium.
Ganguly
A
A
Department of Medicine, Veterans Hospital, Tampa, Florida.
Chiou
S
S
Davis
J S
JS
D000450:Aldosterone / Q000378:metabolism*; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism; D002417:Cattle; D000242:Cyclic AMP / Q000378:metabolism; D003600:Cytosol / Q000378:metabolism; D066298:In Vitro Techniques; D007294:Inositol / Q000378:metabolism; D007295:Inositol Phosphates / Q000302:isolation & purification / Q000378:metabolism*; D007700:Kinetics; D009568:Nitrendipine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D015290:Second Messenger Systems / Q000187:drug effects*; D015384:Zona Glomerulosa / Q000187:drug effects / Q000378:metabolism*
D007295:Inositol Phosphates; D000804:Angiotensin II; D000450:Aldosterone; D007294:Inositol; D009568:Nitrendipine; D000242:Cyclic AMP; D011188:Potassium; D002118:Calcium