Abstract
This study was designed to examine the Ca2+ sensitivity of the contractile system and the ability of the sarcoplasmic reticulum (SR) to accumulate and release Ca2+ in chemically (saponin) skinned cardiac fibers obtained from normal and pressure-overloaded hypertrophied rat left ventricles. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta 6-8 wk before study. Age- and weight-matched normal rats served as controls. Pressure over-load increased the left ventricular weight-to-body weight ratio by 51%. There were no differences in the Ca2+-tension relationship between normal and hypertrophied preparations at Ca2+ concentrations of 10(-7) to 10(-4) M. Caffeine-induced Ca2+ release from the maximally Ca2+ -loaded SR was also not different between the two groups at caffeine concentrations of 0.5-30 mM. However, when the relative amount of Ca2+ accumulated in the SR with 10(-6), 3 x 10(-6), or 10(-5) M Ca2+ loading solutions for various loading periods was estimated by the area under the 25 mM caffeine-induced contraction, the accumulation of Ca2+ was significantly slower in hypertrophied fibers than in normal fibers. We conclude that depressed Ca2+ accumulation by the SR plays a role in modulation of contractile performance in this model of chronic pressure overload in rats.
