In this study, using an animal model of dextran sulfate sodium (DSS)-induced active colitis, we aim to determine the mechanism of colitis-induced atrial electrophysiological remodeling and to test the hypothesis that a colitis-induced increase in AngII/AT1R signaling alters atrial ECG parameters by attenuating atrial conductance and prolonging the APD as a consequence of reduced INa and Ito availability, respectively. This evidence concerns the gene AGTR1 and colitis.