Effects of rhyncophylline (Rhy) on the voltage-dependent potassium channels in isolated rat and guinea pig ventricular myocytes were studied by using patch clamp whole cell recording techniques. Rhy was found to reduce the steady-state outward current in rat ventricular myocytes when cells were depolarized from holding potential -40 mV to 0 mV. After blocking Ca2+ inward current with CdCl2 0.1 mmol/L, a K+ transient outward current (IA) can be recorded. Rhy 30 mumol/L inhibited the IA 30% when depolarized to +50 mV from the holding potential. The delayed outward (IK) and outward tail current (I(tail)) were also reduced 30% and 60%, respectively by Rhy 30 mumol/L which responded to 4.5 sec long pulse from -40 mV to +50 mV. Whereas, the inward rectifying current (IK1) was not changed by Rhy. The present study suggests that the antiarrhythmic action of Rhy was partially due to the K+ channel blocking effects.