Effects of the K+ channel blocker tedisamil on 86Rb efflux induced by cromakalim,high potassium and noradrenaline,and on mechanical tension in rabbit isolated vascular smooth muscle |
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Authors: | Volker A W Kreye Dietmar Pfründer Ursula Theiss |
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Institution: | (1) II. Physiologisches Institut der Universität Heidelberg, Im Neuenheimer Feld 326, W-6900 Heidelberg, Federal Republic of Germany |
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Abstract: | Summary Tedisamil, a new bradycardic agent with an inhibitory action on K+ channels in cardiac muscle, was found to inhibit in a non-competitive manner the relaxation induced by the K+ channel opener cromakalim in noradrenaline-stimulated helical strips from rabbit aortae. Tedisamil tended to be more potent in this respect than glibenclamide; the latter however competitively antagonized the cromakalim-induced relaxation. In rabbit aorta preloaded with 86Rb as a marker of K+, 10 mol/l tedisamil inhibited the 86Rb efflux induced by 10 mol/l cromakalim. — While the 86Rb efflux evoked by depolarization with 100 mmol/l K+ aspartate was inhibited by tedisamil, too, the rise of 86Rb efflux induced by noradrenaline was unaffected by the drug.In non-stimulated rabbit aorta, tedisamil increased mechanical tension in a concentration-dependent manner (EC50 for peak contractions: 32 mol/l; for maintained tension: 24 mol/l), and enhanced 86Rb efflux. Both stimulant actions were antagonized by the calcium antagonist diltiazem.In conclusion, tedisamil affects different K+ channels in vascular smooth muscle. Its stimulant effects are assumed to be secondary to membrane depolarization and subsequent activation of voltage-dependent Ca2+ channels.Supported by the Deutsche Forschungsgemeinschaft
Send offprint requests to V. A. W. Kreye at the above address |
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Keywords: | Cardiovascular agents Diltiazem Glibenclamide K+ channel openers Rabbit aorta |
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