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 extrasystoles. 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.
- Received June 7, 1973.
- Accepted August 28, 1973.
- © 1973 American Heart Association, Inc.