RESUMO
Effects of Mn2+ on isolated guinea pig ventricular myocardia were examined. In isolated papillary muscles, Mn2+ produced a transient decrease in contractile force followed by a late sustained augmentation. Mn2+ markedly increased the amplitude of post-rest contractions; the time course of potentiation was almost the same as that of the late augmentation of contractile force after Mn2+ application. Mn2+ also increased the amplitude of rapid-cooling contractures. The negative inotropic effect of diltiazem and nicardipine was not affected by the presence of Mn2+. Mn2+ shortened the action potential duration under normal condition whereas it prolonged the duration under Ca2+ free conditions. Mn2+, when applied to fura-2-loaded ventricular myocytes, markedly quenched the cytoplasmic fluorescence excited at 360 nm wavelength. We concluded that Mn2+ not only causes a decrease in contractile force by blocking the L-type Ca2+ channel, but also enters the cytoplasm through the channel and produces late augmentation of the contractile force through enhancement of sarcoplasmic reticulum function.