The Exchange Protein directly Activated by cAMP (EPAC) has been implicated in cardiac pro-arrhythmic signalling pathways including spontaneous diastolic Ca$^{2+}$ leak from sarcoplasmic reticulum and increased Action Potential Duration (APD) in isolated ventricular cardiomyocytes. The AP lengthening following acute EPAC activation is mainly due to a decrease of repolarizing steady state K$^+$ current (IK SS ) but the mechanisms involved remain unknown. This study aimed to assess the role of EPAC1 and 2 in the decrease of IK SS and to investigate the underlying signalling pathways. AP and K$^+$ currents were recorded with the whole cell configuration of the patch-clamp technique in freshly isolated rat ventricular myocytes. EPAC1 and 2 were pharmacologically activated with 8-CPTAM (10 µmol/L) and inhibited with R-Ce3F4 and ESI-05, respectively. Inhibition of EPAC1 and EPAC2 significantly decreased the effect of 8-CPTAM on APD and IK SS showing that both EPAC isoforms are involved in these effects. Unexpectedly, CaMKII inhibition by AIP or KN-93, and Ca$^{2+}$ chelation by intracellular BAPTA, did not impact the response to 8-CPTAM. However, inhibition of PLC/PKC and NOS/PKG pathways partially prevents the 8-CPTAM-dependent decrease of IK SS . Finally, the cumulative inhibition of PKC and PKG blocked the 8-CPTAM effect, suggesting that these two actors work along parallel pathways to regulate IK SS upon EPAC activation. On the basis of such findings, we propose that EPAC1 and 2 are involved in APD lengthening by inhibiting a K$^+$ current via both PLC/PKC and NOS/PKG pathways. This may have pathological implications since EPAC is upregulated in diseases such as cardiac hypertrophy.