ArticlePflugers Archiv : European journal of physiology1992
Tedisamil inhibits the delayed rectifier K+ current in single smooth muscle cells of the guinea-pig portal vein.
Article in Pflugers Archiv : European journal of physiology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 29 citations in OpenAlex.
- The inhibitory effects of iberiotoxin and 4-aminopyridine on the relaxation induced by beta 1- and beta 2-adrenoceptor activation in rat aortic rings.British journal of pharmacology · 1996Article
- Regulation of smooth muscle delayed rectifier K+ channels by protein kinase A.Pflugers Archiv : European journal of physiology · 1996Article
- Multiple components of delayed rectifier K+ current in canine colonic smooth muscle.The Journal of physiology · 1995Article
- Levcromakalim-induced modulation of membrane potassium currents, intracellular calcium and mechanical activity in rat mesenteric artery.Naunyn-Schmiedeberg's archives of pharmacology · 1994Article
- Antagonism of levcromakalim by imidazoline- and guanidine-derivatives in rat portal vein: involvement of the delayed rectifier.British journal of pharmacology · 1993Article
- Levcromakalim may induce a voltage-independent K-current in rat portal veins by modifying the gating properties of the delayed rectifier.British journal of pharmacology · 1993Article
- Intracellular ADP activates ATP-sensitive K+ channels in vascular smooth muscle cells of the guinea pig portal vein.Pflugers Archiv : European journal of physiology · 1993Article
- 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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2 authors at 1 institution in 1 country.
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Abstract
Tedisamil is a new bradycardic agent with an inhibitory action on K+ channels in cardiac muscle, and secondary beneficial effects in experimentally induced cardiac ischemia. In whole-cell clamp studies in enzymatically dispersed, single smooth muscle cells from the guinea-pig portal vein, tedisamil inhibited the delayed rectifier K+ current (determined as the charge transferred through the cell membrane), the mean concentration for half-maximal inhibition being 2.9 microM. In contrast to controls in the absence of drugs or in the presence of the classical K+ channel blockers barium, tetraethylammonium or 4-aminopyridine, the time course of the delayed rectifier K+ current in the presence of tedisamil could no longer be fitted by a single exponential, and signs of an accelerated inactivation by tedisamil were obtained. The slow onset of the response to tedisamil applied to the outside of the vascular myocytes, and the finding that tedisamil applied directly to the cytosol via the pipette was highly effective, suggest an intracellular site of action.
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