Alcohol intoxication may induce electrocardiographic changes and arrhythmias, most frequently the atrial fibrillation (AF; e.g. Kodama et al., 2011). Modifications of inward rectifier potassium currents including IK1 have been implicated in the pathogenesis of AF (e.g. Ehrlich, 2008; Wakili et al., 2011). Recently, we have reported that ethanol significantly affects IK1 in rat ventricular myocytes (Bébarová et al., 2013). Nevertheless, data describing the effect of ethanol on the atrial IK1 are still missing. Hence, we aimed to analyse IK1-changes in the presence of ethanol in enzymatically isolated rat atrial myocytes and respective changes of the current in human Kir2.3 channels transiently expressed in Chinese Hamster Ovary (CHO) cells, for comparison. Myocytes were isolated from the atria of adult male Wistar rats (300 ± 10 g) anaesthetised by intramuscular administration of a mixture of tiletamin and zolazepam (65 mg/kg; Zoletil® 100 inj.), and xylazine (20 mg/kg; Rometar® inj.). To digest the atrial tissue, the heart was retrogradely perfused via aorta with nominally Ca2+-free Tyrode solution containing collagenase (type S, Yakult Pharmaceuticals; 0.2 mg/ml), protease (type XIV, Sigma-Aldrich; 0.053 mg/ml) and EGTA (Sigma-Aldrich; 34 μM) in the first step (2.75 min), and, subsequently, with the same solution but without protease (16 min). Experiments were performed by the whole cell patch clamp technique at 23 ± 1°C. In rat atrial cells, a transient inhibition of IK1 by 10.5 ± 2.0 % (13 cells) was observed at the beginning of application of ethanol in a clinically relevant concentration of 80 mM (~3.7‰). The inhibition declined with a delay and, in about half of the cells, it was followed by an activation of the current, at the quasi steady-state by 9.0 ± 1.9 % compared to the control current (7 cells; a representative record is shown in Fig. 1). In our preliminary experiments on the expressed human Kir2.3 channels, 80 mM ethanol induced only an inhibition of the current by 11.5 ± 2.4 % under the same experimental conditions (5 cells; a representative record is shown in Fig. 2). In conclusion, this is the first study demonstrating an effect of ethanol on the atrial IK1. The ethanol effect was apparent in a clinically relevant concentration and partly differed in rat atrial myocytes and in the expressed human Kir2.3 channels. The decline of IK1-inhibition during application of ethanol observed in rat atrial cells along with the following increase of IK1 in a part of these cells may be caused by an unknown mechanism which is not present in the human Kir2.3 channels expressed in CHO cells. Our experimental data suggest that ethanol-induced changes of the atrial IK1 might participate in the reported alterations of atrial electrophysiology under alcohol consumption.