Hypertension is a common cause of heart failure, and ventricular arrhythmias are a major cause of death in heart failure. The Spontaneous Hypertension Heart Failure (SHHF) rat model was used to study altered ventricular electrophysiology in hypertension and heart failure. We hypothesized that a reduction in the inward rectifier K⁺ (I_K1and expression of pacemaker (I_f) current would favor abnormal automaticity in the SHHF ventricle. SHHF ventricular myocytes were isolated at two and eight months of age, and during end-stage heart failure (seventeen months); myocytes from age-matched rats served as controls. Inward I_K1 was significantly reduced at both eight and seventeen months in SHHFs compared to controls. There was a reduction in inward I_K1 due to aging in the controls only at >seventeen months. We found a significant increase in I_f at all ages in the SHHFs, compared to young controls. In controls, there was an age-dependent increase in I_f. Action potential recordings in the SHHFs demonstrated abnormal automaticity, which was abolished by the addition of an I_f blocker (10 µM zatebradine). Increased I_f during hypertension alone, or combined increases in I_f with reduced I_K1 during the progression to hypertensive heart failure, contribute to a substrate for arrhythmogenesis.