کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5986832 | 1178866 | 2010 | 9 صفحه PDF | دانلود رایگان |
The aim of this study was to determine the effects of desethyl-amiodarone (DEA), the major metabolite of the class III antiarrhythmic drug amiodarone, on human ether-à -go-go-related gene (hERG) encoded potassium channel current.Materials and methodsWhole-cell patch clamp recordings were made at 37°C of ionic current (IhERG) carried by recombinant hERG channels expressed in HEK-293 cells.ResultsDesethyl-amiodarone inhibited IhERG with a half-maximal inhibitory concentration of approximately 158 nmol/L, compared with approximately 47 nmol/L for amiodarone. The inhibitory action of DEA on IhERG was contingent on channel gating, showing significant time and voltage dependence. Desethyl-amiodarone also produced an approximately â9 mV shift in the voltage dependence of activation of IhERG; however, there was no significant preference for activated over inactivated channels.ConclusionsBecause hERG underlies native cardiac “IKr” channels, hERG/IKr inhibition by DEA as well as amiodarone may contribute to the overall effects of amiodarone administration on cardiac repolarization.
Journal: Journal of Electrocardiology - Volume 43, Issue 5, SeptemberâOctober 2010, Pages 440-448