Abstract:
AIM To study the effects of bepridil on the rapidly activating component (
IKr), the slowly activating component (
IKs) of the delayed rectifier potassium current and the inward rectifier potassium current (
IK1) 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
IKr and
IKs (by 20.9% and 27.2% at 0 mV and +50 mV, respectively). The effect of bepridil on
IKs was larger than on
IKr. Bepridil 30 μmol·L
-1 also significantly inhibited the inward component of
IK1(by 15.1% at +100 mV), but the reverse potential of
IK1 was unaffected. Bepridil (1-100 μmol·L
-1 ) was shown to inhibit
IKr and
IKs in a concentration-dependent manner. Their IC
50 were 46.7 μmol·L
-1 and 23.8 μmol·L
-1, respectively. CONCLUSION Bepridil inhibit
IKr,
IKs and
IK1 in hypertrophied guinea pig ventricular myocytes, which may be important in understanding the antiarrhythmic effects of this drug.