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AJP - Renal Physiology, Vol 251, Issue 6 1055-F1062, Copyright © 1986 by American Physiological Society
ARTICLES |
C. S. Park, T. W. Honeyman, E. S. Chung, J. S. Lee, D. H. Sigmon and J. C. Fray
This study sought to elucidate further the cellular mechanism(s) involved in the control of renin secretion by Ca2+. The rate of renin secretion in vitro by rabbit and dog renal cortical slices was inversely related to medium Ca2+ concentration. The inverse relationship was observed only when the cell membrane permeability to Ca2+ was increased by K+ depolarization, suggesting that the Ca2+ concentration in the juxtaglomerular cell modulates renin secretion. From this relationship, renin secretion appears to turn on at intracellular Ca2+ concentrations between 10(-8) and 10(-7) M. Calmidazolium, a potent calmodulin antagonist, markedly stimulated basal renin secretion in a concentration-dependent manner. Pretreatment of slices with calmidazolium blocked the inhibition of renin secretion by high-K+ medium. Calmidazolium and several other calmodulin antagonists (W-7, W-13, and trifluoperazine) partly or fully reversed the inhibition of renin secretion previously inhibited by high-K+ medium in the order of their potencies as calmodulin antagonists. Indeed, W-5, a biologically inactive structural analogue of W-7, was without effect. These results support the hypothesis that renin secretion is inversely related to intracellular Ca2+ and that Ca2+ inhibits renin secretion by a calmodulin-dependent process.
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M. C. Ortiz-Capisano, P. A. Ortiz, P. Harding, J. L. Garvin, and W. H. Beierwaltes Decreased Intracellular Calcium Stimulates Renin Release via Calcium-Inhibitable Adenylyl Cyclase Hypertension, January 1, 2007; 49(1): 162 - 169. [Abstract] [Full Text] [PDF] |
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