Abstract
1. Glibenclamide, a sulphonylurea oral hypoglycaemic agent is a widely used antagonist of cromakalim-activated K+ channels in smooth muscle. 2. In isolated ring segments of the large circumflex coronary artery from the dog, glibenclamide (1-30 microM) caused a concentration-dependent reduction in both spontaneous isometric force and contractions induced by U46619, a thromboxane A2-mimetic. 3. Glibenclamide behaved as a competitive antagonist of U46619 with an estimated pKB (-log KB) value of 6.2 by Schild regression analysis (slope 1.07). 4. Glibenclamide (30 microM) was apparently selective since it had no effect on the concentration-contraction curves to endothelin-1, noradrenaline or KCl. 5. We suggest that this additional property of glibenclamide should be considered in any smooth muscle study where active force is raised by either the exogenous application or endogenous generation of thromboxane A2.
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