Antiarrhythmic and bradycardic drugs inhibit currents of cloned K+ channels, KV1.2 and KV1.4

We investigated the effects of the antiarrhythmic drugs, quinidine, disopyramide, flecainide, clofilium, verapamil, and the bradycardic drug, bertosamil, on the currents of the cloned K+ channels, KV1.2 (IK(V1.2)) and KV1.4 (IK(V1.4)), using the Xenopus oocyte expression system. Both IK(V1.2) and IK...

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Bibliographic Details
Published in:European journal of pharmacology 1995-08, Vol.281 (2), p.151-159
Main Authors: YAMAGISHI, T, ISHII, K, TAIRA, N
Format: Article
Language:English
Subjects:
Animals
Anti-Arrhythmia Agents - pharmacology
Antiarythmic agents
Biological and medical sciences
Bradycardia - etiology
Cardiovascular system
Cloning, Molecular
Disopyramide - pharmacology
Dose-Response Relationship, Drug
Mathematics
Medical sciences
Oocytes
Pharmacology. Drug treatments
Potassium Channels - drug effects
Quaternary Ammonium Compounds - pharmacology
Quinidine - pharmacology
Verapamil - pharmacology
Xenopus laevis
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Summary:We investigated the effects of the antiarrhythmic drugs, quinidine, disopyramide, flecainide, clofilium, verapamil, and the bradycardic drug, bertosamil, on the currents of the cloned K+ channels, KV1.2 (IK(V1.2)) and KV1.4 (IK(V1.4)), using the Xenopus oocyte expression system. Both IK(V1.2) and IK(V1.4) were inhibited in a concentration-dependent manner by quinidine (10 microM to 1 mM), flecainide (10 microM to 1 mM), clofilium (10-300 microM), verapamil (10 microM to 1 mM) and bertosamil (10 microM to 1 mM) but not by disopyramide (10 microM to 1 mM). The inhibitory effects of clofilium, verapamil and bertosamil on IK(V1.2) were time-dependent. The decay time course of IK(V1.4) was accelerated by clofilium, verapamil and bertosamil, but decelerated by quinidine and flecainide. These results indicate that IK(V1.2) and IK(V1.4) are targets for the four antiarrhythmic drugs and the bradycardic drug.
ISSN:0014-2999
1879-0712
DOI:10.1016/0014-2999(95)00240-L