Objective. We investigated the effects of WXKL on the action potential (AP) and the L-type calcium current (I Ca-L) in normal and hypertrophied myocytes. Methods. Forty male rats were randomly divided into two groups: the control group and the transverse aortic constriction- (TAC-) induced heart failure group. Cardiac hypertrophy was induced by TAC surgery, whereas the control group underwent a sham operation. Eight weeks after surgery, single cardiac ventricular myocytes were isolated from the hearts of the rats. The APs and I Ca-L were recorded using the whole-cell patch clamp technique. Results. The action potential duration (APD) of the TAC group was prolonged compared with the control group and was markedly shortened by WXKL treatment in a dose-dependent manner. The current densities of the I Ca-L in the TAC group treated with 5 g/L WXKL were significantly decreased compared with the TAC group. We also determined the effect of WXKL on the gating mechanism of the I Ca-L in the TAC group. We found that WXKL decreased the I Ca-L by accelerating the inactivation of the channels and delaying the recovery time from inactivation. Conclusions. The results suggest that WXKL affects the AP and blocked the I Ca-L, which ultimately resulted in the treatment of arrhythmias.