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1 Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States; Biophysics Program, Ohio State University, Columbus, Ohio, United States
2 David Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States
3 College of Pharmacy, Ohio State University, Columbus, Ohio, United States
4 Davis Heart and Lung Research Institute, The Ohio State University, Columbus, Ohio, United States; College of Pharmacy, Ohio State University, Columbus, Ohio, United States
* To whom correspondence should be addressed. E-mail: carnes.4{at}osu.edu.
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+ (IK1and expression of pacemaker (If) 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 IK1 was significantly reduced at both eight and seventeen months in SHHFs compared to controls. There was a reduction in inward IK1 due to aging in the controls only at >seventeen months. We found a significant increase in If at all ages in the SHHFs, compared to young controls. In controls, there was an age-dependent increase in If. Action potential recordings in the SHHFs demonstrated abnormal automaticity, which was abolished by the addition of an If blocker (10 µM zatebradine). Increased If during hypertension alone, or combined increases in If with reduced IK1 during the progression to hypertensive heart failure, contribute to a substrate for arrhythmogenesis.
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