| Autor: |
Kreye, Volker, Pfründer, Dietmar, Theiss, Ursula |
| Zdroj: |
Naunyn-Schmiedeberg's Archives of Pharmacology; 1992, Vol. 345 Issue 2, p238-243, 6p |
| Abstrakt: |
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 Rb as a marker of K, 10 μmol/l tedisamil inhibited the Rb efflux induced by 10 μmol/l cromakalim. - While the Rb efflux evoked by depolarization with 100 mmol/l K aspartate was inhibited by tedisamil, too, the rise of Rb efflux induced by noradrenaline was unaffected by the drug. In non-stimulated rabbit aorta, tedisamil increased mechanical tension in a concentration-dependent manner (EC for peak contractions: 32 μmol/l; for maintained tension: 24 μmol/l), and enhanced Rb 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 Ca channels. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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