Effects of benzyltetrahydropalmatine on potassium currents in guinea pig and rat ventricular myocytes.

AIM: To investigate the effects of benzyltetrahydropalmatine (BTHP) on rapidly
activating component (I(Kr)), slowly activating component (I(Ks)) of delayed
rectifier potassium current, inward rectifier potassium current (I(K1)), and
transient outward potassium current (I(to)) in single ventricular myocytes.
METHODS: Whole-cell patch clamp technique was used to record ionic currents.
RESULTS: (1) BTHP 30 micromol/L reduced I(Kr) and I(Kr,tail) by 31 %+/-4 % and 36
%+/-5 % (n=6, P <0.01), respectively and inhibited I(Ks) and I(Ks,tail) by 40
%+/-6 % and 45 %+/-5 % (n=7, P <0.01), respectively. I(Kr) and I(Ks) were blocked
by BTHP 1-100 micromol/L in a concentration-dependent fashion (IC50 value was
13.5 micromol/L and 95 % confidence limit: 11.2-15.8 micromol/L for I(Kr), 9.3
micromol/L and 95 % confidence limit: 7.8-11.8 micromol/L for I(Ks),
respectively). (2) BTHP 5 micromol/L inhibited I(to) by 63 %+/-6 % (n=6, P
<0.01). BTHP 1-100 micromol/L reduced I(to) in a concentration-dependent manner
(IC50 value was 3.6 micromol/L and 95 % confidence limit: 2.9-4.3 micromol/L).
(3) BTHP 200 micromol/L did not affect I(K1).
CONCLUSION: BTHP inhibited I(Kr), I(Ks), and I(to), but not I(K1). The
antiarrhythmic effects of BTHP may be mainly due to its blockade on potassium
channels.