Steady state outward K+ currents (IKss) show very rapid activation and relatively slow or no inactivation and therefore contribute outward current throughout phases 1,2 and the early part of phase 3 of the action potential (AP). They are thought to be important in cardiac cell types with abbreviated plateau phases (Choisy et al. 2004). Inwardly rectifying background K+ currents (e.g. IK1) regulate membrane excitability as well as contributing to the late phases of action potential repolarisation. Both these currents have been suggested to be under noradrenergic control (Ravens et al. 1989, Fedida et al. 1991). More recently, noradrenaline (NA) has been shown to have biphasic effects on resting membrane potential in rat left atrial and pulmonary vein preparations (Doisne et al. 2009). At present, however, there are no published data describing the modulation of these currents by NA in rat atrial cardiomyocytes. The present study was designed to investigate noradrenergic modulation of the steady state K+ outward current and inward rectifying current in rat atrial cardiomyocytes. Male Wistar rats (200-320 g) were anaesthetised with an intra-peritoneal injection of sodium pentobarbital (60-100 mg/kg). The heart was then rapidly excised, mounted on a Langendorff apparatus and retrogradely perfused via the aorta with a series of solutions at 37 oC as previously described (Choisy et al. 2004). The left atrium was then removed, finely chopped and triturated in Kraftbrühe (KB) solution. Ionic currents were recorded in whole cell voltage clamp mode using a standard external Tyrode’s solution and K+-based pipette solution. Cardiomyocytes were held at a holding potential of -80 mV and a ramp protocol applied every 3 s: a step to +20 mV for 100 ms was followed by a ramp to -120 mV over 500 ms. IKss was measured as the steady-state outward current at +20 mV and IK1 was measured as the K+-dependent inward current at -120 mV. Current voltage relations were analyzed by repeated measures two way ANOVA with Bonferroni post hoc test (p<0.05 was considered significant). NA (1 μM) significantly inhibited the steady state outward current at +20 mV but was without effect on IK1 at -120 mV (n=6). This inhibition was unaffected in the presence of atenolol (1 μM, n=7), prazosin (5 μM, n=7) or atenolol plus prazosin (n= 7). On the other hand, in the presence of propranalol (1 μM) the inhibitory effect of NA on steady state outward K+ current was abolished (n=5). Furthermore the steady state outward K+ current was significantly inhibited by the β2-adrenoceptor-selective agonist, zinterol (1 μM) in the presence of atenolol (1 μM) (n=5).These data suggest that the steady state outward K+ current in rat atrial cardiomyocytes is modulated by NA via the β2 adrenoceptor.