Abstract: OBJECTIVE To study the effects of orientin(Ori) on the sodium channel currents(I_Na) of ventricular myocardial cells in rats, and to explore its anti-arrhythmic mechanisms at the ion channel level. METHODS Ventricular myocardial cells were enzymatically isolated from rats by Langendorff with constant pressure and temperature. The whole-cell patch clamp techniques were used to observe the changes of I_Na at different concentrations of ori. RESULTS There was no significant effect on I_Na, when the concentration of Ori was <2 μmol·L^-1. I-V curve of I_Nasignificantly moved up under the influence of 3, 10 and 30 μmol·L^-1 Ori, and the peak sodium current(I_Na-Peak)was reduced from (-81.49±3.9)pA/pF to (-74.38±4.1)pA/pF, (-63.05±2.8)pA/pF and (-55.35±3.2)pA/pF. Ori moved the steady-state activation curve of I_Na to the right, the steady-state inactivation curve to the left, and the recovery curve to the right. The half activation voltage(V_1/2-ac)changed from (-53.66±4.12)mV to (-44.64±1.9)mV, (-38.95±1.7)mV and (-30.21±1.5)mV. The half inactivation voltage(V_1/2-in)changed from (-51.68±0.76)mV to (-60.17±1.5)mV, (-68.51±1.4)mV and (-75.22±1.37)mV. And the recovery time(τ)changed from (18.38±0.84)ms to (24.53±1.4)ms, (35.25±1.3)ms and (68.75±1.58)ms. CONCLUSION Ori block I_Na of rat ventricular myocytes in a concentration-dependent manner. It also has a significant effect on the kinetics characteristics of activation, inactivation and the recovery.