A carrier mechanism that mediates an exchange of Na+ for Ca2+ across the cell membrane is believed to be an important regulator of intracellular Ca2+ and therefore the contractile strength of the heart. Considerable evidence indicates that there is an unequal transfer of electrical charge during this exchange which implies that the carrier may contribute substantially to the net flow of ionic current across the sarcolemmal membrane. To detect such a component of current, nondialyzed single frog atrial cells were transiently Ca2+-loaded by augmenting Ca2+ entry through membrane Ca2+ channels by exposure to either the beta-adrenergic agonist, isoproterenol, or to BAY K 8644, a Ca2+ channel agonist. A direct comparison of whole-cell Ca2+ currents during exposure to these compounds in Na+-containing and Na+-free solutions revealed the existence of an additional component of inward current in Na+-containing solutions which temporally overlaps with Ca2+ channel-mediated currents. The dependence of this component of inward current on intracellular Ca2+ and extracellular Na+ and its resemblance to previously characterized carrier-mediated currents (creep currents) in this preparation suggest that it is associated with electrogenic Na+-Ca2+-exchange activity. These experiments support earlier predictions that under some conditions a component of the slow inward current in the heart may actually represent Ca2+ efflux mediated by an electrogenic Na+-Ca2+-exchange carrier.