Isolated infant human atrial cells have a slower early repolarization than adult human atrial cells. In addition, from room temperature voltage-clamp studies, infant cells have lower basal L-type calcium currents than adult cells. We hypothesized that the slower repolarization increases the calcium transient of infant human atrial cells. Atrial myocytes were enzymatically dissociated from biopsies of human right atrial appendages of infant (3-8 mo) patients who were undergoing open-heart surgery. Intracellular calcium transients were measured with fluorescence microscopy with application of either square waves or action potential waveforms at physiologic temperature. After repetitive application (1 Hz) of 100-ms duration conditioning depolarizations to 10 mV (from -80 mV), a test pulse of varying duration (DeltaT; 2-100 ms) produced smaller transients (expressed as percentage of the last conditioning pulse) at shorter durations (33 +/- 7% for DeltaT = 2 ms, 80 +/- 4% for DeltaT = 25 ms). With repetitive application of either adult or infant prerecorded action potentials to infant cells, the cells had a decreased calcium transient with the adult action potential (F/F(0) 2.2 +/- 0.4 for infant action potential versus 1.6 +/- 0.2 for adult action potential; n = 7; p < 0.05). The delayed early repolarization of infant cells alters the Ca(2+) transient, which may compensate for the lower availability of basal calcium current in infant cells. The steep relationship that we have demonstrated between test-pulse duration and the calcium transient suggests that modulation of the early repolarization phase of the action potential may be of great significance in modulating excitation-contraction coupling.