Intracellular mediators of potassium-induced aldosterone secretion

Arunabha Ganguly; Shirley Chiou; John S. Davis

doi:10.1016/0024-3205(90)90102-W

Intracellular mediators of potassium-induced aldosterone secretion

Arunabha Ganguly, Shirley Chiou, John S. Davis

Research output: Contribution to journal › Article › peer-review

13 Scopus citations

Abstract

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.

Original language	English (US)
Pages (from-to)	173-180
Number of pages	8
Journal	Life Sciences
Volume	46
Issue number	3
DOIs	https://doi.org/10.1016/0024-3205(90)90102-W
State	Published - 1990
Externally published	Yes

ASJC Scopus subject areas

General Pharmacology, Toxicology and Pharmaceutics
General Biochemistry, Genetics and Molecular Biology

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10.1016/0024-3205(90)90102-W

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title = "Intracellular mediators of potassium-induced aldosterone secretion",

abstract = "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.",

author = "Arunabha Ganguly and Shirley Chiou and Davis, {John S.}",

note = "Funding Information: This work was supported by the Veterans Administration and the American Heart Association (Florida Affiliate). The authors wish to thank Dr. Alexander Scriabine of Miles Laboratory for providing the nitrendipine used in this study and Ms. Linda Sagun for typing the manuscript.",

year = "1990",

doi = "10.1016/0024-3205(90)90102-W",

language = "English (US)",

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pages = "173--180",

journal = "Life Sciences",

issn = "0024-3205",

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T1 - Intracellular mediators of potassium-induced aldosterone secretion

AU - Ganguly, Arunabha

AU - Chiou, Shirley

AU - Davis, John S.

N1 - Funding Information: This work was supported by the Veterans Administration and the American Heart Association (Florida Affiliate). The authors wish to thank Dr. Alexander Scriabine of Miles Laboratory for providing the nitrendipine used in this study and Ms. Linda Sagun for typing the manuscript.

PY - 1990

Y1 - 1990

N2 - 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.

AB - 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.

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JO - Life Sciences

JF - Life Sciences

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ER -

Intracellular mediators of potassium-induced aldosterone secretion

Abstract

ASJC Scopus subject areas

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