Bradykinin does not mediate activation of glucose transport by muscle contraction

Abstract

The purpose of this study was to evaluate the report that bradykinin is the “muscle activity hypoglycemia factor” responsible for the activation of glucose transport that occurs in response to muscle contractile activity. Stimulation of rat epitrochlearis muscles to contract resulted in approximately a fourfold increase in the rate of intracellular accumulation of the nonmetabolizable glucose analog 3-O-methylglucose. Incubation of the muscles with high concentrations of aprotinin (Trasylol), a polypeptide inhibitor of kallikrein which blocks formation of kinins, did not inhibit the activation of sugar transport by contractile activity. Furthermore incubation of muscles with bradykinin did not have a stimulatory effect on the uptake of 3-methylglucose either at a physiological concentration or at high concentrations. These results provide no support for the claims that aprotinin prevents the activation of sugar transport in muscle by contractile activity or that bradykinin is the muscle activity hypoglycemia factor.