["The Journal of Physiology, EarlyView. ", "\nAbstract figure legend The ultrarapid delayed rectifier potassium current (IKur) has long been considered an atrial‐specific current with no functional role in the ventricles, despite evidence of its expression in ventricular myocytes. In the present study we challenged this prevailing concept and investigated the potential role of IKur in ventricular repolarization. Cellular electrophysiology and molecular cardiology experiments were performed on cardiac preparations obtained from dog and undiseased human hearts. We show clear evidences that IKur current is present in the ventricular myocardium at both molecular and functional levels. We confirm the presence of IKur current in atrial and ventricular tissue using immunochemistry, standard microelectrode and patch‐clamp techniques. We also confirm that IKur current plays a significant role in ventricular repolarization reserve, as under conditions where the repolarization reserve was pharmacologically attenuated (by inhibiting IKr current), additive inhibition of IKur induces early afterdepolarizations (EADs), indicating that its blockade might have a significant proarrhythmic side effect.\n\n\n\n\n\n\n\n\n\nAbstract\nThe ultrarapid delayed rectifier potassium current (IKur) has long been considered an atrial‐specific current with no functional role in the ventricles, despite evidence of its expression in ventricular myocytes. In the present study we challenged this prevailing concept and investigated the potential role of IKur in ventricular repolarization. Kv1.5 protein expression was determined by immunocytochemistry in canine and undiseased human cardiac tissue samples. Action potentials (APs) were recorded using conventional microelectrode techniques in canine and human cardiac preparations, and ion currents were measured using the whole‐cell patch‐clamp technique in isolated cardiomyocytes. In silico simulations were performed to investigate the role of the IKur current using a human ventricular model (T‐WorldIKur). Kv1.5 protein expression was detected in canine atrial, ventricular and Purkinje fibre cells, as well as in undiseased human left ventricular myocardium. In canine atrial preparations IKur inhibition shifted the plateau phase of the AP into the positive voltage direction and consequently shortened AP duration. Application of 100 µM 4‐aminopyridine (4‐AP) revealed ionic currents of similar magnitude in ventricular myocytes and Purkinje fibres, which were attributed to IKur. Inhibition of IKur caused prolongation of the APs recorded from endocardial and midmyocardial preparations, as well as from Purkinje fibres. Under conditions of attenuated repolarization reserve IKur inhibition induced augmented repolarization lengthening and frequent early afterdepolarizations (EADs). In silico modelling data regarding the IKur inhibition‐evoked EAD formations are in good agreement with the experimental findings. IKur is present and functionally active in ventricular myocardium and may represent a significant contributor to ventricular repolarization reserve.\n\n\n\n\n\n\n\n\n\nKey points\n\nThe ultrarapid delayed rectifier potassium current (IKur) has long been considered an atrial‐specific current with no functional role in the ventricles.\nIn the present study, we challenged this prevailing concept and investigated the potential role of IKur in ventricular repolarization. Cellular electrophysiology and molecular cardiological experiments were performed on cardiac preparations obtained from dog and undiseased human hearts.\nWe present clear evidence that IKur current is present in the ventricular myocardium at both molecular and functional levels. We also confirm that IKur current plays a significant role in ventricular repolarization reserve.\nWe concluded that IKur is present and functionally active in ventricular myocardium and may represent a significant contributor to ventricular repolarization reserve.\n\n\n"]