Key result
Pressure-overload hypertrophy in rats caused slower twitch relaxation (force half-time 83 vs 68 ms) and [Ca2+]i decline (time constant 208 vs 118 ms), suggesting decreased SR Ca2+-ATPase function.
Why the study?
Does pressure-overload left ventricular hypertrophy alter force and Ca2+ handling in isolated rat myocardium?
Does pressure-overload left ventricular hypertrophy alter force and Ca2+ handling in isolated rat myocardium?
Pressure-overload hypertrophy in rats is associated with slower twitch relaxation and Ca2+ decline, likely due to decreased SR Ca2+-ATPase function contributing to diastolic dysfunction.
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May contribute to diastolic dysfunction mechanisms in hypertrophy; leaves open translation to human pressure-overload LVH.
Maier et al. (1998) studied Left ventricular hypertrophy. Banding of the abdominal aorta vs. Control animals was evaluated on Isometric force and intracellular free Ca2+ concentration ([Ca2+]i). Pressure-overload hypertrophy in rats caused slower twitch relaxation (force half-time 83 vs 68 ms) and [Ca2+]i decline (time constant 208 vs 118 ms), suggesting decreased SR Ca2+-ATPase function.
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