Abstract
In the isolated rabbit heart, verapamil reduced the rate of rise and the slope of diastolic slow depolarization, the maximum, diastolic potential (Ed) and the membrane potential at the peak of depolarization (Ea) of the SA node without preventing regenerative responses in ventricular and Purkinje fibers. This effect of verapamil on SA node was counteracted by raising the extra-cellular calcium ion concentration. On the other hand, tetrodotoxin (TTX) had almost no effect on these parameters of the SA node, but it reduced the maximum rate of rise of the ventricular and Purkinje fibers markedly and eventually rendered these tissues non-excitable. The difference in the actions of verapamil and TTX on the SA node suggests that the SA nodal action potential comes from a different ionic channel (slow channel) from that of the Purkinje fibers or the working myocardium, and the effect of calcium ion suggests that this ion plays an important role in the generation of the SA nodal action potential. The difference in the effect of verapamil on the repolarization phase between ventricular and Purkinje fibers was pointed out and the possible participation of calcium ion in the repolarization phase of these two tissues was discussed.
