心肌肽素对豚鼠心室肌细胞钠通道的影响

Effects of cardiomyopeptidin on sodium current in ventricular myocytes of guinea pigs

目的:研究心肌肽素对豚鼠心室肌细胞钠通道的影响,探讨心肌肽素在离子通道水平的作用机制。方法:用急性酶解分离法获得豚鼠心室肌细胞,标准全细胞膜片钳技术记录钠电流(INa)。结果:心肌肽素1、5、10、50、100、500 mg/L使豚鼠心室肌细胞INa分别减少(0±1)%、(6±2)%、(10±2)%、(15±1)%、(22±9)%、(30±6)%,呈浓度依赖性抑制INa。心肌肽素50 mg/L使INa激活时间(TTP)从(2.8±0.7)m s延长至(3.0±0.8)m s(P<0.05);使INa电流密度-电压曲线上移,但不改变激活电位、峰电位、反转电位和I-V曲线的形状;不影响稳态激活曲线、稳态失活曲线和稳态失活后恢复曲线。结论:心肌肽素浓度依赖性抑制豚鼠心室肌细胞INa,可能是其抗心律失常作用的机制之一。

AIM： To determine the effect of cardiomyopeptidin on sodium current （ INa ） in ventrieular myocytes of guinea pigs and to explore the mechanism of cardiomyopeptidin action at the ionic channel level. METHODS： Single ventricular myocytes of guinea pigs were obtained by enzymatic dissociation method. The whole - cell patch - clamp recording technique was used to record the change of INa. RESULTS： Cardiomyopeptidin （ 1, 5, 10, 50, 100 and 500 mg/L） decreased INa in a dose - dependent manner. The inhibition rates were （ 0 ± 1 ） %, （ 6 ± 2 ） %, （ 10 ± 2 ） %, （ 15 ± 1 ） %, （22 ± 9） % and （ 30 ± 6） %, respectively. The time to peak （TTP） was delayed from （ 2. 8 ± 0. 7 ） ms to （3.0 ± 0. 8 ） ms （ P 〈 0. 05 ） by cardiomyopeptidin （ 50 mg/L） , In the presence of cardiomyopeptidin （ 50 mg/L）, the current density - voltage curve of INa was shifted and without change of its active potential, peak potential, reversal potential, and the shape of the curve. The steady activation curve, the steady inactivation curve and the steady inactivation recovery curve of INa were not affected. CONCLUSION： Cardiomyopeptidin inhibits the INa in guinea pig ventricular myocytes, which may be one of the mechanisms of its antiarrhythmic effect.