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Insulin Inhibits Dog Vascular Smooth Muscle Contraction and Lowers Ca²⁺_i by Inhibiting Ca²⁺ Influx¹

University of Texas Medical School, Houston, TX 77030

Essential hypertension, obesity and non-insulin-dependent diabetes are associated with resistance to insulin-induced glucose disposal. Because physiological concentrations of insulin inhibit vascular smooth muscle (VSM) contraction in vivo, it has been proposed that resistance to insulin-induced inhibition of VSM contraction might be partly responsible for the elevated vascular resistance found in these clinical conditions. Nevertheless, it is not known how insulin inhibits contraction of normal VSM. Several workers have demonstrated that insulin attenuates the agonist-induced intracellular Ca²⁺ (Ca²⁺_i) transient in VSM, although the identity of the sarcolemmal and/or sarcoplasmic reticular Ca²⁺ transport systems that are affected by insulin is controversial. Our laboratory has examined the effects of a physiological concentration of insulin on contraction and Ca²⁺ transport in cultured VSM cells from canine femoral artery. We have found that insulin inhibits agonist-induced contraction and attenuates the agonist-induced Ca²⁺_i transient by inhibiting Ca²⁺ influx, but not by increasing Ca²⁺ efflux or inhibiting Ca²⁺ release from internal stores. Insulin also stimulates ouabain-sensitive ⁸⁶Rb⁺ uptake (Na⁺-K⁺ pump activity) and does not inhibit VSM contraction in the presence of ouabain. Our data support the hypothesis that insulin stimulates Na⁺-K⁺ pump activity, resulting in hyperpolarization of the cell and decreased Ca²⁺ influx via voltage-operated channels.

KEY WORDS: • hypertension • diabetes • obesity • serotonin • Na⁺-K⁺ pump

¹ Presented as part of the symposium "Insulin Resistance, Obesity and Hypertension" given at the Experimental Biology '94 meeting, Anaheim, CA, on April 27, 1994. This symposium was sponsored by the American Institute of Nutrition. Guest editor for this symposium was Michael B. Zemel, The University of Tennessee, Knoxville, TN.

² To whom correspondence should be addressed: University of Texas Medical School, P.O. Box 20708, Houston, TX 77030.

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