Abstract

The effects of batrachotoxin (BTX) on the electrogenic properties of Purkinje fibers isolated from the dog heart were studied with intracellular techniques. BTX caused a depolarization of the Purkinje fiber membrane and in a few cases the membrane potential reached values of +20 mV. Application of anodal hyperpolarizing current, 1 mM Na-sucrose solution or tetrodotoxin to the Purkinje fiber previously depolarized by BTX, restored the membrane potential to values similar to control conditions. High extracellular calcium concentration prolonged the time course of the BTX effect but did not prevent it. Prior to the onset of membrane depolarization, BTX caused an increase in the duration of the plateau and negative afterpotential of the action potential. Simultaneous with the depolarization induced by BTX, a decremise in the upstroke velocity and overshoot of the spike potential occurred together with an increase in the rate of depolarization during the diastolic interval. When the membrane was depolarized to values less than -20 mV. excitability was lost. These effects of BTX on heart Purkinje fibers were antagonized by tetrodotoxin. The results raise the possibility of the existence of functionally different sodium channels. It is concluded that BTX acts on the heart Purkinje fiber to selectively increase sodium permeability.