Background and aim: Atrial fibrillation (AF) is the most common chronic/recurrent arrhythmia, which significantly impairs quality of life, increases cardiovascular morbidity and mortality. Previous results showed that inhibition of acetylcholine sensitive potassium current (IK,Ach) may represent a novel, atrial-specific target for the management of AF in chronic AF (1,2). Therefore, the aim of the present study was to investigate the properties of three repolarizing potassium currents, which contribute to AF-induced electrical remodelling, in isolated atrial myocytes obtained from dogs either with sinus rhythm (SR) or following chronic atrial tachypacing induced AF-dogs. Methods: Atrial remodelling and AF were induced by chronic (4-6 weeks) right atrial tachypacing (400/min) in dogs. Transmembrane ionic currents were measured by applying the whole-cell patch clamp technique at 37°C. AF was induced by short bursts (800/min). Results: The transient outward current (Ito) current was slightly downregulated in AF cells when compared with that recorded in SR cells. This downregulation was also associated with slowed inactivation kinetics. Inward rectifier potassium current (IK1) current was found to be larger in AF cells. IK,ACh was activated by the cholinergic agonist carbachol (CCh; 2 µM). In SR, CCh activated a large current either in inward or outward directions. The selective IK,ACh inhibitor tertiapin (10 nM) blocked the outward CCh-induced current by 61.3±2.3% (n=5; *p<0.05). In atrial cardiomyocytes isolated from dogs with AF, the presence of a constitutively active IK,ACh was observed, blocked by 59.4±3,5% (n=5, *p<0,05) with 10 nM tertiapin. However, in ‘AF atrial myocytes’, CCh activated an additional, significant ligand-dependent and tertiapin-sensitive IK,ACh current. Tertiapin Q significantly and dose dependently reduced AF incidence and AF episode duration, prolonged atrial effective refractory period (ERP) and action potential duration (APD). Conclusions: In our dog AF model, Ito unlike in human was downregulated only in a slight manner. Due to its slow inactivation kinetics, it seems that Ito may play a more significant role in atrial repolarization than in ventricular working muscle myocytes. The presence of the constitutively active IK,ACh in atrial myocytes from AF dogs shows that electrical remodelling truly developed in this model. The IK,ACh current (both ligand-dependent and constitutively active) seems to play a significant role in canine atrial electrical remodelling, and may be a promising atrial selective drug target for suppressing AF.