Effects of taurine-magnesium coordination compound on sodium channel in rat cardiomyocytes of arrhythmia induced by aconitine / 中国药理学通报

ABSTRACT

Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination compound on sodium current in single rat ventricular myocytes of arrhythmia induced by aconitine.Methods Whole-cell patch clamp was used to record INa in normal cardiomyocytes and single rat ventricular cardiomyocytes of arrhythmia induced by aconitine.Results In ventricular cardiomyocytes of rat,INa was blocked by 100~400 ?mol?L-1 TMCC in a concentration-dependent manner.INa was increasd from(45.56?1.96)pA/pF to(59.19?11.49)pA/pF by 1 ?mol?L-1 aconitine,while decreased to(34.23?1.33)pA/pF by 24.24 ?mol?L-1 amiodarone.TMCC(100,200,400 ?mol?L-1)could restore INa to(51.61?5.96)pA/pF,(40.91?6.73)pA/pF,(41.50?5.50)pA/pF respectively.Amiodarone could restore INa to(40.22?1.47)pA/pF.Conclusions TMCC can restore INa,which is increased by aconitine,and the effect is equal to that of amiodarone.TMCC blocks INa of ventricular cardiomyocytes,which may be one of its antiarrhythmic mechanisms.