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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 M²+ 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% (APD_30) and 90% repolarization (APD_90), especially showing a tendency towards more remarkable prominent shortening in APD_30 than APD_90. Cooling from 337 to 33 and 27˚C 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 veraparnil and imipramine significantly attenuated the increasing [Mg²+]o induced APD shortening in both APD_30 and APD_90 whereas the [Mg²+]o induced APD shortening was not affected by strophanthidin, glibenclamide and tetrabutylammonium. These findings suggest that 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+.
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