Altered calcium handling at normal contractility in hypertrophied rat heart.

Left or right ventricular hypertrophy was induced by banding of the aorta or pulmonary artery in different groups of rats. After 5 to 10 weeks the degree of hypertrophy was about 15% in left and 80-160% in right ventricles, as determined by weight of the ventricle or by myocyte size. Action potentials and force-interval relationships were measured in papillary muscles isolated from either ventricle. As compared to muscles from control and SHAM-operated rats, hypertrophied papillary muscles showed: (1) Marked prolongation of the action potential and greater degree of post-extrasystolic potentiation. This indicates enhanced influx of Ca2+ probably via Ica; (2) Delayed relaxation of isometric force and faster decay of potentiation, which indicates reduced sequestration of Ca2+ by the sarcoplasmic reticulum; (3) Minor changes in steady-state peak force under standard conditions, which is explained from the opposite inotropic effects of enhanced Ca2+ influx and impaired function of the reticulum. Myocyte volume in the normal left ventricle was almost two times larger than in the normal right ventricle, and this was associated with a longer action potential and greater degree of post-extrasystolic potentiation in left as compared with right ventricular muscles. The rate of decay of potentiation, however, was not different. This might indicate that depressed function of the sarcoplasmic reticulum occurs with pressure-overload hypertrophy and not with normal age-dependent growth.