Effect of calcium on acetylstrophanthidin induced transient depolarizations in canine Purkinje tissue

The role of calcium ions (Ca²⁺) in the generation of transient depolarizations (TDs) by acetylstrophanthidin was examined. Transmembrane activity was recorded from isolated canine false tendons exposed to acetylstrophanthidin; concentrations from 7.5 x 10^-8 to 2 x 10^-7 g/ml caused TDs coupled to driven action potentials and depressed slow diastolic depolarization. TDs could reach threshold and induce extra systoles. Elevation of the Ca²⁺ concentration increased the amplitude of TDs induced by acetylstrophanthidin. High Ca²⁺ concentration (12.5 mM) caused TDs and depression of slow diastolic depolarization in the absence of acetylstrophanthidin. Elevation of potassium (K⁺) concentration depressed and reduction of K⁺ concentration potentiated TDs caused by either acetylstrophanthidin or high Ca²⁺ concentration. The production of TDs and the depression of slow diastolic depolarization by acetylstrophanthidin were reversed by reduction of the Ca²⁺ concentration or addition of manganese (2 mM) to the superfusing Tyrode's solution. The results suggest that TDs and arrhythmias produced by acetylstrophanthidin may be caused by a transient Ca²⁺ influx.