Rats harboring the human renin and angiotensinogen genes (dTGR) feature angiotensin (Ang) II/hypertension-induced cardiac damage and die suddenly between week 7 and 8. We observed by ECG telemetry that ventricular tachycardia (VT) is a common terminal event in these animals. Our aim was to investigate electrical remodeling. We used ECG telemetry, non-invasive cardiac magnetic field mapping (CMFM) at week 5 and 7, and performed in-vivo programmed electrical stimulation at week 7. We also investigated whether or not losartan (Los; 30 mg/kg/d) would prevent electrical remodeling. Cardiac hypertrophy and systolic blood pressure progressively increased in dTGR, compared to Sprague-Dawley (SD) controls. Already by week 5, untreated dTGR showed increased perivascular and interstitial fibrosis, connective tissue growth factor expression, and monocyte infiltration compared to SD rats, differences that progressed through time. Left ventricular (LV) mRNA expression of potassium channel subunit Kv4.3 and gap junction protein Cx43 were significantly reduced in dTGR compared to Los-treated dTGR and SD. CMFM showed that depolarization and repolarization were prolonged and inhomogeneous. Los ameliorated all disturbances. VT could be induced in 88% of dTGR, but only in 33% of Los-treated dTGR and could not be induced in SD. Untreated dTGR show electrical remodeling and probably die from VT. Los treatment reduces myocardial remodeling and predisposition to arrhythmias. Ang II target organ damage induces VT.