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We have investigated the effect of extracellular Mg2+ ([Mg2+]o) on action potential duration (APD) in guinea pig papillary muscles by using microelectrodes. Increasing [Mg2+]o resulted in progressive negative inotropic effect, progressive ascending depolarization of membrane potential, and increase in intracellular Mg2+ concentration. In addition, increase in [Mg2+]o from 1.1 to 3, 6, 10, and 20 mM produced a reversible dose-dependent shortening of both APD at 30% (APD30) and 90% repolarization (APD90), especially showing a tendency towards more remarkable prominent shortening in APD30 than APD90. Cooling from 37 to 33 and 27℃ diminished the [Mg2+]o-induced APD shortening. Increase in extracellular Ca2+ concentration from 1.8 to 3.6 and 5.4 mM caused a significant depressed effect on the increasing [Mg2+]o-induced APD shortening. Furthermore, increase in [Mg2+]o from 1.1 to 10 and 20 mM produced a significant depressed effect on the APD shortening induced by extracellular Ca2+. Pretreatment of verapamil and imipramine significantly attenuated the increasing [Mg2+]o-induced APD shortening in both APD30 and APD90, whereas the [Mg2+]o-induced APD shortening was not affected by strophanthidin, glibenclamide and tetrabutylammonium. These findings suggest that the effects of [Mg2+]o on APD are probably due to a decrease in ionic transport across plasma membrane. In conclusion, the present study indicates that [Mg2+]o exerts antiarrhythmic activities by antagonistic actions on intracellular Ca2+.