Presence and functional role of the rapidly activating delayed rectifier K+ current in left and right atria of adult mice

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 (IKr) in left and right atrial myocytes of mouse heart, using whole-cell patch-clamp method. The functional role of ultrarapid delayed rectifier (IKur) in the repolarization was also examined by blocking with 4-aminopyridine (50 μM). The presence of IKr was detected in left and right atrial myocytes as an E-4031 (5 μM)-sensitive current that exhibited relatively rapid activation during depolarization and half activation voltage of −17.5 and −17.4 mV for left and right atrial myocytes, respectively. The current density of IKr 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 IKur 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 IKur, is likely to enhance the functional significance of IKr in repolarization process of right atrium, despite of similar magnitude of IKr in left and right atria. Our data thus identifies IKr in mouse atria and indicates the presence of functional interaction between IKr and IKur that potentially contributes to repolarization heterogeneity in left and right atria of mouse heart.