Steady state outward K+ currents (IKss) activate rapidly on depolarisation, show little inactivation and are thought to be important in action potential repolarisation. In ventricular myocytes, IKss has been suggested to be under adrenergic control (Choisy et al. 2004, Ravens et al. 1989, Scamps 1996). At present, however, there are no published data describing a noradrenaline (NA) -sensitive IKss in atrial myocytes. This study was designed to characterise IKss and investigate its modulation by NA in atrial myocytes. Procedures were approved by the Ethics Committee of the University of Bristol and were conducted in accordance with UK legislation. Male Wistar rats were anaesthetised by sodium pentobarbital (60-100 mg/kg i.p.) and left atrial myocytes isolated from the excised heart as previously described (Choisy et al. 2004). Ionic currents were recorded in whole cell voltage clamp mode using an external Tyrode’s solution and K+-based pipette solution. Superfusion of cells with 1 μM NA potentiated the L-type Ca2+ current (ICaL) at 0 mV by 205±39.7 % and inhibited IKss at +50 mV by 44±4.6 % (p≤0.001, Student’s paired t-test, n=6). While the effect of NA on ICaL was abolished by the β1-antagonist atenolol (10 μM), the inhibition of IKss was unaffected. The inhibitory action of NA on IKss was also unaffected by the α1-antagonist, prazosin (5 μM), or atenolol plus prazosin. However, in the presence of the β1/β2-antagonist, propranolol (1 μM), the NA-induced inhibition of IKss was abolished. Furthermore, the action of NA on IKss was mimicked by the β2-agonist, zinterol (1 μM) in the presence of atenolol (10 μM). The steady state outward current was markedly reduced and the inhibitory effect of NA lost when recordings were made under K+-free conditions, indicating the involvement of a K+-selective current. NA reduced the power of the noise of IKss. Power spectral analysis of the NA-sensitive current indicated a single channel conductance of 27.6±5.1 pS (n=14). The NA-sensitive current was partially inhibited by 4-aminopyridine (3 mM). The action of NA on IKss in rat atrial myocytes was abolished in pertussis toxin-treated cells. The effect on action potential duration (APD) of IKss inhibition by NA was examined in the presence of 10 μM atenolol to prevent changes in ICaL. In cells stimulated at 1 Hz, 1 μM NA prolonged APD30 by 17±5.4 % (P≤0.05, Student’s paired t-test, n=8) but had no effect on APD60 or APD90. In summary, these data demonstrate the existence of a steady state K+ current that plays a role in modulation of APD by NA via a pertussis toxin-sensitive β2-adrenoceptor mediated pathway in rat atrial cells.