Effects of toosendanin (TS) on the action potentials and contractile force in guinea pig papillary muscles were examined using a standard microelectrode technique. TS concentration-dependently increased the action potential duration at 90% repolarization (APD90) of the fast action potentials. In the presence of a Ikl channel blocker BaCl2, the effects of TS on lengthening the APD90 were completely abolished, thereby suggesting that TS inhibited the inward rectifier K+ current Ikl. The APD and contractile force of aminophylline-induced slow action potentials were potentiated by TS in a concentration-dependent manner. In the presence of BaCl2, both effects of TS were completely abolished. Thus, TS selectively inhibited the inward rectifier K+ current Ikl with a positive inotropic effect, resulting from a delay in Ca channel inactivation which was secondary to delay in ventricular repolarization
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