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

The role of calcium ions (Ca) 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"" to 2 X 10-" g/ml caused TDs coupled to driven action potentials and depressed slow diastolic depolarization. TDs could reach threshold and induce extrasystoles. Elevation of the Caconcentration increased the amplitude of TDs induced by acetylstrophanthidin. High Ca+ concentration (12.5 ITIM) 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 Ca+ concentration. The production of TDs and the depression of slow diastolic depolarization by acetylstrophanthidin were reversed by reduction of the Ca concentration or addition of manganese (2 ITIM) to the supervising Tyrode's solution. The results suggest that TDs and arrhythmias produced hy acetylstrophanthidin may be caused by a transient Ca ' influx.