Renin-angiotensin (RAS) system activation is associated with an increased risk for sudden death. Previously, we constructed a mouse model of RAS activation using cardiac-restricted angiotensin converting enzyme (ACE) overexpression. These mice, termed ACE 8/8, die prematurely and abruptly. Here, we investigated cardiac electrophysiological abnormalities that may contribute to early mortality in this model. ACE 8/8 mice have reduced surface electrocardiographic voltages. Intracardiac electrograms showed a- and v-potential amplitudes of 11% and 24% when compared to matched wild-type (WT) controls. The atrioventricular (AV), atrio-Hisian (AH), and Hisian-ventricular (HV) intervals were prolonged 2.8, 2.6, and 3.9 fold in ACE 8/8 versus WT. Various degrees of AV nodal block were present only in ACE 8/8 mice. By intracardiac electrophysiology studies, WT and heterozygote (HZ) mice were noninducible, whereas 83% of ACE 8/8 mice demonstrated ventricular tachycardia with burst pacing. Compared to WT, ACE 8/8 mice showed reductions in atrial connexin 40 (Cx40) and connexin 43 (Cx43) protein levels, ventricular Cx43 protein level, atrial and ventricular Cx40 mRNA abundances, ventricular Cx43 mRNA abundance, and atrial and ventricular cardiac sodium channel (Scn5a) mRNA abundances. Additionally, ACE 8/8 mice demonstrated ventricular Cx43 dephosphorylation. Atrial and ventricular L-type calcium channel, Kv4.2 potassium channel alpha-subunit, and connexin 45 mRNA abundances and the peak ventricular sodium current did not differ between the groups. In isolated heart preparations, a connexin blocker, 1-heptanol (0.5 mmol/L), produced a similar electrophysiological phenotype to that seen in ACE 8/8 mice. Therefore, cardiac-specific ACE overexpression resulted in changes in connexins consistent with the phenotype of low voltage electrical activity, conduction defects, and induced ventricular arrhythmia. These results may help explain the increased risk of arrhythmia in states of RAS activation such as heart failure.