BEPRIDIL INHIBITION ON THE DELAYED RECTIFIER K⁺ CURRENTS IN THYROXINE INDUCED HYPERTROPHIED GUINEA PIG VENTRICULAR MYOCYTES

AIM To study the effects of bepridil on the rapidly activating component (I_Kr), the slowly activating component (I_Ks) of the delayed rectifier potassium current and the inward rectifier potassium current (I_K1) in hypertrophied guinea pig ventricular myocytes. METHODS The whole cell patch clamp techniques were used. RESULTS In hypertrophied guinea pig ventricular myocytes, bepridil 30 μmol·L^-1 markedly inhibited I_Kr and I_Ks (by 20.9% and 27.2% at 0 mV and +50 mV, respectively). The effect of bepridil on I_Ks was larger than on I_Kr. Bepridil 30 μmol·L^-1 also significantly inhibited the inward component of I_K1(by 15.1% at +100 mV), but the reverse potential of I_K1 was unaffected. Bepridil (1-100 μmol·L^-1 ) was shown to inhibit I_Kr and I_Ks in a concentration-dependent manner. Their IC₅₀ were 46.7 μmol·L^-1 and 23.8 μmol·L^-1, respectively. CONCLUSION Bepridil inhibit I_Kr, I_Ks and I_K1 in hypertrophied guinea pig ventricular myocytes, which may be important in understanding the antiarrhythmic effects of this drug.