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AJP - Endocrinology and Metabolism, Vol 268, Issue 5 E1027-E1030, Copyright © 1995 by American Physiological Society
ARTICLES |
C. Yang and W. H. Hsu
Department of Veterinary Physiology and Pharmacology, Iowa State University, Ames, Iowa 50011, USA.
Rat pancreas perfusion was performed to study the effect of bradykinin on insulin release. At the perfusate glucose concentration of 6 mM, bradykinin (0.01-1 microM) increased insulin release in a concentration-dependent manner. In addition, bradykinin (1 microM) increased the glucose (10 mM)-induced insulin release. HOE-140 (0.1 microM), a bradykinin B2-receptor antagonist, decreased the baseline insulin release and abolished the bradykinin (1 microM)-induced increase in insulin release. In addition, HOE-140 (0.1 microM) attenuated the glucose (10 mM)-induced increase in insulin release. Because the blockade of bradykinin receptors by HOE-140 attenuated the glucose-induced increased insulin release, our present findings suggest that bradykinin may play a physiological role in the regulation of insulin release.
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