Although the genetics of mammalian cardiac K+ channels have been most intensively investigated in mice, there are limited data available from the electrophysiological studies of the K+ currents in native mouse cardiac myocytes, especially in fetal mouse heart. The present study utilized whole cell patch-clamp techniques to assess the delayed rectifier K+ current (IK) in fetal (18th day of gestation) mouse ventricular myocytes. IK in fetal mouse ventricular myocytes activated rapidly, displayed a negative slope conductance of the current-voltage relationships at test potentials > 0 mV, satisfied the envelope of IK-tail test for a single component, and was very sensitive to dofetilide. These characteristics confirm that this current is the rapidly activating component of IK known as IK,r. In addition, dofetilide dramatically prolonged action potential duration in single ventricular myocytes as well as in ventricular myocardium, suggesting that IK,r plays a dominant role in action potential repolarization in fetal mouse heart. From these data we can conclude that fetal mouse cardiac myocytes express IK,r, which functions as a dominant repolarizing K+ current.