Purkinje fibers from dog hearts may have either a "high" resting potential of about -90 mV or a "low" resting potential of about -40 mV when immersed in low-Cl(-) solution containing 4 mM K(+). Brief exposure of Purkinje fibers at the low level of resting potential to K(+)-free fluid causes further depolarization, and return to K(+)-containing solution elicits a transient hyperpolarization which reaches a peak within a few seconds and then declines within a few minutes. Repeating these changes in K(+) concentration after clamping the membrane potential at its steady resting level in K(+)-containing fluid allows the changes in net membrane current presumably underlying the depolarization and transient hyperpolarization to be measured. Net inward current is recorded when the fiber is exposed to K(+)-free solution, and a transient net outward current arises when it is returned to K(+)-containing solution. The transient net outward current reflects a temporary increase in the rate of electrogenic Na(+) extrusion caused by the rise in intracellular Na(+) concentration that occurs while the sodium pump is slowed in K(+)-free fluid. Sodium extrusion remains enhanced, presumably until the internal Na(+) concentration has been brought back to its resting level. The transient outward current is completely abolished by the cardiac steroid acetylstrophanthidin, and its amplitude is increased as the prior exposure to K(+)-free fluid is prolonged. The decay of the transient outward current and the decline in intracellular Na(+) concentration both appear to follow first-order kinetics.