Abstract: The effects of isocorydine on the action potentials of rabbit sinoatrial node and guinea pig ventricular muscles as well as the spontaneous electrical activity induced by barium ion in ventricular muscles were studied with intracellular microelectrodes. When the sinoatrial node cells were exposed to 30 μM or 300 μM isocorydine, their APA, SP₀, SP₄ were decreased. Concomitantly, isocorydine slowed the rate of spontaneous impulse initiation by the sinoatrial node. At the concentration of 3 μM, isocorydine prolonged the durations of action potential (APD₅₀, APD₉₀)and the effective refractory period (ERP) of the ventricular muscle cells. A prolongation of ERP was observed with 30 μM isocorydine, without any significant effects on other parameters of action potential. By raising the concentration to 300 μM, isocorydine caused an obvious shortening of the duration of action potential but not ERP. Isocorydine 300 μm can also efficiently suppress the spontaneous electriccal activity induced by barium ion in guinea pig ventricular muscles.