Repolarization of cardiac action potentials is regulated by several types of K + currents. The present study examined the presence and functional significance of rapid delayed rectifier (I Kr ) in left and right atrial myocytes of mouse heart, using whole-cell patch-clamp method. The functional role of ultrarapid delayed rectifier (I Kur ) in the repolarization was also examined by blocking with 4-aminopyridine (50μM). The presence of I Kr was detected in left and right atrial myocytes as an E-4031 (5μM)-sensitive current that exhibited relatively rapid activation during depolarization and half activation voltage of −17.5 and −17.4mV for left and right atrial myocytes, respectively. The current density of I Kr was similar between left and right atria. The prolongation of action potential measured at 50% repolarization evoked by 4-aminopyridine was significantly larger in left than in right atrium, which appears to be consistent with the larger amplitude of I Kur in left atrium. On the other hand, the prolongation of action potential measured at 90% repolarization caused by E-4031 was significantly larger in right than in left atrium. The longer action potential of right atrium, which may result at least partly from smaller amplitude of I Kur , is likely to enhance the functional significance of I Kr in repolarization process of right atrium, despite of similar magnitude of I Kr in left and right atria. Our data thus identifies I Kr in mouse atria and indicates the presence of functional interaction between I Kr and I Kur that potentially contributes to repolarization heterogeneity in left and right atria of mouse heart.