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Am J Physiol Cell Physiol 256: C368-C374, 1989;
0363-6143/89 $5.00
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AJP - Cell Physiology, Vol 256, Issue 2 C368-C374, Copyright © 1989 by American Physiological Society

ARTICLES

Insulin-induced hyperpolarization in mammalian skeletal muscle

S. T. Iannaccone, K. X. Li, N. Sperelakis and D. A. Lathrop
Department of Neurology, University of Cincinnati Medical Center, Ohio 45267.

Insulin-induced hyperpolarization of up to 9 mV has been described in isolated frog [J. Physiol. Lond. 252: 43-58, 1975; Am. J. Physiol. 251 (Cell Physiol. 4): C249-C254, 1979] and mammalian (Molecular Basis of Insulin Action, New York: Plenum, 1985, p. 451-463; Am. J. Physiol. 197: 524-526, 1959; Am. J. Physiol. 198: 1066-1070, 1960) skeletal muscle. We have shown that a similar hyperpolarization occurs in situ after administration of insulin in anesthetized rats. In streptozotocin (STZ)-treated rats, insulin produced approximately 66-70% of the hyperpolarization observed in normal rat skeletal muscle in situ. Administration of ouabain in situ blocked the insulin-induced hyperpolarization in the normal group of rats and significantly blunted the effect in the STZ group. These results suggest that insulin-induced hyperpolarization in skeletal muscle results from direct activation of the Na+-K+-ATPase pump. In isolated skeletal muscle from normal and STZ rats, there was no difference in the amount of the insulin-induced hyperpolarization. There was an additive, but small, hyperpolarizing effect of insulin and isoproterenol when administered in combination, suggesting that the greater magnitude of the insulin-induced hyperpolarization observed in situ in normal rats may be due to an additive effect of injected insulin and endogenous release of epinephrine. Alternatively, STZ treatment may directly alter the Na+-K+ pump so that its response to insulin is lessened.


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