TY - JOUR
T1 - Greater importance of Ca2+-calmodulin in maintenance of ang II-and K+-mediated aldosterone secretion
T2 - Lesser role of protein kinase C
AU - Ganguly, Arunabha
AU - Chiou, Shirley
AU - Fineberg, Naomi S.
AU - Davis, John S.
N1 - Funding Information:
Acknowledgments. These studies were supported by grants from the Medical Research Funds of the Veterans Administration and American Heart Association (Florida affiliate). Authors wish to thank Dr. Alexander Scriabine of Miles Laboratories for providing the nttrendipine and Ms. Linda Sagun for typing the manuscript.
PY - 1992/1/15
Y1 - 1992/1/15
N2 - In this study we have investigated various components of the stimulus-secretion coupling process leading to aldosterone secretion from the calf adrenal glomerulosa cells as evoked by angiotensin II (AII) and potassium (K+). The roles of Ca2+, calmodulin and protein kinase C in the sustained phase rather than initiation of aldosterone secretion were of special interest. Our investigations revealed that the reduction of extracellular Ca2+ by EGTA or interruption of Ca2+ influx by nitrendipine at various time points after stimulation with either AII or K+ markedly compromised aldosterone secretion. Calmodulin inhibitors, calmidazolium and W-7 reduced aldosterone secretion profoundly. Agonists of protein kinase C, phorbol ester or diacylglycerol analogues failed to stimulate aldosterone secretion while the protein kinase C inhibitor, H-7, only partially inhibited aldosterone secretion at a concentration which completely inhibited protein kinase C activity. Calmodulin inhibitors produced significantly greater inhibition of aldosterone secretion than inhibitors of protein kinase C.
AB - In this study we have investigated various components of the stimulus-secretion coupling process leading to aldosterone secretion from the calf adrenal glomerulosa cells as evoked by angiotensin II (AII) and potassium (K+). The roles of Ca2+, calmodulin and protein kinase C in the sustained phase rather than initiation of aldosterone secretion were of special interest. Our investigations revealed that the reduction of extracellular Ca2+ by EGTA or interruption of Ca2+ influx by nitrendipine at various time points after stimulation with either AII or K+ markedly compromised aldosterone secretion. Calmodulin inhibitors, calmidazolium and W-7 reduced aldosterone secretion profoundly. Agonists of protein kinase C, phorbol ester or diacylglycerol analogues failed to stimulate aldosterone secretion while the protein kinase C inhibitor, H-7, only partially inhibited aldosterone secretion at a concentration which completely inhibited protein kinase C activity. Calmodulin inhibitors produced significantly greater inhibition of aldosterone secretion than inhibitors of protein kinase C.
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U2 - 10.1016/S0006-291X(05)80138-X
DO - 10.1016/S0006-291X(05)80138-X
M3 - Article
C2 - 1731785
AN - SCOPUS:0026528964
SN - 0006-291X
VL - 182
SP - 254
EP - 261
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
IS - 1
ER -