Non-uniform Electrophysiological Properties and Electrotonic Interaction in Hypertrophied Rat Myocardium

• Published in: Circulation research Vol. 49; no. 1; pp. 150 - 158
• Main Authors: KEUNG, EDMUND C.H, AHONSON, RONALD S
• Format: Journal Article
• Language: English
• Published: United States American Heart Association, Inc 01.07.1981
• Subjects: Action Potentials; Animals; Blood Pressure; Cardiomegaly - etiology; Cardiomegaly - physiopathology; Electrodes; Electrophysiology; Heart - anatomy & histology; Hypertension, Renal - complications; Male; Membrane Potentials; Organ Size; Papillary Muscles - physiopathology; Rats
• ISSN: 0009-7330; 1524-4571
• DOI: 10.1161/01.res.49.1.150

We studied the distribution and nature of the electrical changes associated with myocardial hypertrophy induced by renal hypertension in rats. Standard microelectrode techniqueB were used to study transmembrane action potentials recorded from endocardial, papillary muscle, and epicardial fibers from hypertrophied (HBP) and normal (SHAM) hearts. We also determined the effects of stimulation frequency on the action potentials recorded from these preparations. To assess whether altered intercellular electrical connections contribute to the electrophygiological changes associated with hypertrophy, we analyzed the spatial steady state voltage decrement produced by passing intracellular constant current pulses and determined the effective input resistance (R) of endocardial HBP and SHAM preparations. Our results show that the action potential prolongation that accompanies hypertrophy is not uniform. Thus, the entire course of repolarization is prolonged in endocardial and papillary muscle fibers, but only the latter half of repolarization is prolonged in epicardial fibers. Endocardial action potentials in general, and HBP action potentials in particular, have a distinctive steep relation between duration and stimulation frequency which may be due to a difference in the rate dependence of a membrane conductance(s), although relatively greater accumulation of extracellular potassium or altered activity of the Na-K pump cannot be excluded as contributing factors. In addition, the similarity in the profile of spatial voltage decrement and the values for R in HBP and SHAM preparations indicates that alterations in electrotonic coupling between cells are unlikely to account for the prolonged action potentials of hypertrophied myocardium.