The potassium transient outward current (Ito) is activeonly during the early plateau of the action potential (AP) and, therefore, its role in governing APD is controversial. The goal of this work is to characterize Ito from patchclamp experiments in canine ventricular epicardial cells and demonstrate its influence in cardiac restitution using an AP mathematical model. Data from our experiments has been used to define a new mathematical model for Ito, which has been then inserted in the Decker et al. model for canine epicardial AP, substituting the original formulation of Ito. The new model predicts an increase in action potential duration (APD) when Ito is blocked, in accordance with recent experimental evidence. Inspection of the ionic currents in the simulations show that the blockade of Ito may indirectly affect other plateau ionic currents like L-type Calcium current (ICaL) and the rapid component of the rectifier potassium current (IKr), producing an increment in the APD. These novel findings emphasize the importance of I to in repolarization and suggest a potential role of Ito blockade in arrhythmogenesis.