Activation of the sodium pump blocks the growth hormone-induced increase in cytosolic free calcium in rat adipocytes

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Department of Physiology

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Adipocytes; Animals; Biological Transport; Bumetanide; Calcium; Cells, Cultured; Cytosol; Enzyme Activation; Growth Hormone; Insulin; Kinetics; Male; Models, Biological; Nimodipine; Ouabain; Rats; Rubidium; Sodium-Potassium-Exchanging ATPase


Life Sciences | Medicine and Health Sciences


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 microM 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.


Endocrinology. 2000 Feb;141(2):513-9.

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