(Hypertension. 1996;28:209-212.)
© 1996 American Heart Association, Inc.
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the First Department of Internal Medicine (M.I., T.I., N.O., H.M., M.W., G.K.) and Department of Clinical Laboratory Medicine (M.K., T.O.), Hiroshima (Japan) University School of Medicine.
Correspondence to Tetsuya Oshima, MD, Department of Clinical Laboratory Medicine, Hiroshima University School of Medicine, 1-2-3 Kasumi, Minami-ku, Hiroshima 734, Japan.
The influence of insulin on platelets in vitro has not been exhaustively investigated. To clarify whether insulin affects Ca2+ metabolism in platelets directly or through alteration of other systems regulating intracellular Ca2+ homeostasis, we examined the effect of insulin both alone and in combination with prostaglandin E1 on platelet aggregation and Ca2+ metabolism. Incubation of rat platelets with insulin reduced thrombin-induced Ca2+ influx but did not change thrombin-evoked release of Ca2+ from internal stores or the size of internal Ca2+ stores. The interactive effects of insulin with prostaglandin E1 were only additive, and insulin did not augment the effects of prostaglandin E1 on platelet Ca2+ metabolism. In contrast, insulin did not inhibit thrombin-induced platelet aggregation but did augment inhibition of platelet aggregation by prostaglandin E1. Our results suggest that insulin inhibits platelet function by both prostaglandin E1dependent and -independent mechanisms.
Key Words: insulin calcium prostaglandins platelet aggregation
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