苄基四氢巴马汀对豚鼠心室肌细胞快激活延迟整流钾电流的作用(英文)

EFFECTS OF BENZYLTETRAHYDROPALMATINE ON THE RAPIDLY ACTIVATING COMPONENT OF DELAYED RECTIFIER POTASSIUM CURRENT IN GUINEA PIG VENTRICULAR MYOCYTES

目的 研究苄基四氢巴马汀 (BTHP)对心室肌细胞快激活 (Ikr)延迟整流钾电流的作用。方法用全细胞膜片钳技术记录豚鼠心室肌细胞钾离子通道电流。结果 BTHP在 1～ 10 0 μmol·L-1以浓度依赖性方式阻滞Ikr,其IC50 为 13 5 μmol·L-1(95 %可信范围 :11 2～ 15 8μmol·L-1)。 30 μmol·L-1BTHP可使Ikr及Ikr,tail分别降低 (31± 4 ) %和 (36± 5 ) % (n =6 ,P <0 0 1)。与多数III类抗心律失常药物不同 ,BTHP可频率依赖性地抑制Ikr。该药主要改变Ikr的失活过程 ,可使Ikr的失活时间常数 (τ)从 (2 38± 16 )ms降至 (196± 14 )ms ,而对Ikr的激活动力学影响不大。结论 BTHP对Ikr有明显的抑制作用 。

AIM To investigate the effect of benzyltetrahydropalmatine (BTHP) on the rapidly activating component of delayed rectifier K + current ( I kr ) in single guinea pig ventricular myocytes. METHODS Whole cell patch clamp technique was used to record I kr . RESULTS I kr was blocked by 1～100 μmol·L -1 BTHP in concentration , voltage , and specifically frequency dependent fashion, with IC 50 of 13 5 μmol·L -1 (95% confidence range: 11 2～15 8 μmol·L -1 ). 30 μmol·L -1 BTHP reduced I kr and I kr,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 I kr,tail . CONCLUSION BTHP inhibited I kr in a frequency dependent fashion.