ArticleNaunyn-Schmiedeberg's archives of pharmacology1992
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.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- Effects of tedisamil (KC-8857) on cardiac electrophysiology and ventricular fibrillation in the rabbit isolated heart.British journal of pharmacology · 1996Article
- Tedisamil inhibits the delayed rectifier K+ current in single smooth muscle cells of the guinea-pig portal vein.Pflugers Archiv : European journal of physiology · 1992Article
- 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.Naunyn-Schmiedeberg's archives of pharmacology · 1992Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 mumol/l tedisamil inhibited the 86Rb efflux induced by 10 mumol/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 mumol/l; for maintained tension: 24 mumol/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.
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