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Endocrinology Vol. 141, No. 2 513-519
Copyright © 2000 by The Endocrine Society


ARTICLES

Activation of the Sodium Pump Blocks the Growth Hormone-Induced Increase in Cytosolic Free Calcium in Rat Adipocytes1

Shikha Gaur2, Hiroshi Yamaguchi3 and H. Maurice Goodman

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655

Address all correspondence and requests for reprints to: Dr. H. Maurice Goodman, Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655. E-mail: maurice.goodman{at}umassmed.edu

GH promptly increases cytosolic free calcium ([Ca2+]i) in freshly isolated rat adipocytes. Adipocytes deprived of GH for 3 h or longer are incapable of increasing [Ca2+]i in response to GH, but instead respond in an insulin-like manner. Insulin blocks the GH-induced increase in [Ca2+]i in GH-replete cells and stimulates the sodium pump (i.e. Na+/K+-ATPase), thereby hyperpolarizing the cell membrane. Blockade of the Na+/K+-ATPase with 100 µM ouabain reversed these effects of insulin and enabled GH to increase [Ca2+]i in GH-deprived adipocytes. Both insulin and GH activated the sodium pump in GH-deprived adipocytes, as indicated by increased uptake of 86Rb+. Decreasing availability of intracellular Na+ by blockade of Na+/K+/2Cl- symporters or Na+/H+ antiporters abolished the effects of both hormones on 86Rb+ uptake and enabled both GH and insulin to increase [Ca2+]i in GH-deprived adipocytes. The data suggest that hormonal stimulation of Na+/K+-ATPase activity interferes with activation of voltage-sensitive calcium channels by either membrane hyperpolarization or some unknown interaction between the sodium pump and calcium channels.




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A Kidson, F J Rubio-Pomar, A Van Knegsel, H T A Van Tol, W Hazeleger, D W B Ducro-Steverink, B Colenbrander, S J Dieleman, and M M Bevers
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