EFFECTS OF ANTIARRHYTHMIC AND BRADYCARDIAC DRUGS ON CLONED CARDIAC K+ CHANNELS

We investigated the effects of the antiarrhythmic drugs, quinidine, disopyramide, flecainide: clofilium, and verapamil, and the bradycardic drug, bertosamil, on the currents of the cloned K+ channels, K-V1.2 (a delayed rectifier type, I-K(V1.4)) and K-V1.4 (a transient outward type, I-K(V1.4)), expressed in Xenopus oocytes by the two-microelectrode voltage-clamp method. Both I-K(V1.2) and I-K(V1.4)two-microelectrode voltage-clamp method. Both I-K(V1.2) and I-K(V1.4) were inhibited in a concentration-dependent manner by quinidine (0.01-1 mM), flecainide (0.01-1 mM), clofilium (10-300 mu M), verapamil (0.01-1 mM), and bertosamil (0.01-1 mM), but not by disopyramide (0.01-1 mM). These results suggest that I-K(V1.2) and I-K(V1.4) are targets for the antiarrhythmic drugs, quinidine, flecainide, clofilium, and verapamil, and for the bradycardic drug bertosamil.