Cardiac-specific overexpression of wild-type 1B-adrenergic receptors (₁-AR) in mice predisposes to dilated cardiomyopathy and sudden death. Although -adrenergic stimulation is thought to contribute to induction of arrhythmias in heart failure, the electrophysiological consequences of chronic 1-adrenergic activation have not been clearly defined. Thus, we characterized ventricular repolarization and monitored incidence of spontaneous arrhythmias in end-stage heart failure ₁-AR mice (9-12 months) and younger ₁-AR mice (2-3 months) that do not present signs of heart failure. ECG recordings revealed that older ₁-AR mice exhibited spontaneous ventricular arrhythmias. Compared to aged matched controls, the QTc interval was 34% longer in the 9-12 months ₁-AR mice and the action potential durations were also significantly prolonged in these mice. These changes were associated with a decrease in the density of the outward K⁺ currents I_to, I_Kur and I_ss (at +30 mV, reduction of 68%, 64% and 41%, respectively) and underlying K⁺ channel expression. These changes can contribute to the rhythm abnormalities observed in the ₁-AR mice and are likely caused by chronic ₁-AR activity. Additional data obtained in 2-3 months ₁-AR mice clearly showed that electrical remodeling was already observed in younger transgenic animals. However, it appeared to be slightly less pronounced than in older mice. These results suggest that there are two waves of remodeling, one due to chronic ₁-adrenergic receptor activity and a second due to heart failure. Taken together, these data provide strong evidence for a pathological role of chronic ₁-AR activity in the development of repolarization defects and ventricular arrhythmias.