Abstract: AIM To investigate the effect of benzyltetrahydropalmatine (BTHP) on the rapidly activating component of delayed rectifier K+ current (Ikr) in single guinea pig ventricular myocytes. METHODS Whole-cell patch clamp technique was used to record Ikr. RESULTS Ikr was blocked by 1~100 μmol*L-1 BTHP in concentration-, voltage-, and specifically frequency-dependent fashion, with IC50 of 13.5 μmol*L-1 (95% confidence range: 11.2~15.8 μmol*L-1). 30 μmol*L-1 BTHP reduced Ikr and Ikr,tail by (31±4)% and (36±5)% (n=6, P<0.01), respectively. The time constant for deactivation (τ′) of the tail current was decreased by 30 μmol*L-1 BTHP from (238±16) ms to (196±14) ms, while drug had no any effect on the time constant for activation (τ) of Ikr,tail. CONCLUSION BTHP inhibited Ikr in a frequency-dependent fashion.