Key result
Isoproterenol-induced cardiac hypertrophy in rats was associated with significantly enhanced contractile force driven by altered intracellular calcium handling, with no change in calcium sensitivity.
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In a rat model of isoproterenol-induced cardiac hypertrophy, enhanced contractile force is driven by altered intracellular calcium handling rather than changes in myofilament calcium sensitivity.
OBJECTIVE: To study the calcium-dependent mechanisms contributing to altered contractile function in isoproterenol-induced ventricular hypertrophy of the rat heart. DESIGN: The force-interval relationship, systemic evaluation of changed contractile force and calcium sensitivity of the myofilaments were investigated using small trabecular muscle from hearts with isoproterenol-induced cardiac hypertrophy. METHODS: Cardiac hypertrophy was induced by daily subcutaneous injection of isoproterenol for 12 days. The calcium sensitivity of myofilaments was studied using non-ionic detergent (Triton-X-100)-skinned trabeculae. The contractile force was evaluated at various concentrations of extracellular calcium and muscle lengths. The force-interval relationship was used to reflect altered intracellular calcium handling. RESULTS: The isoproterenol-induced cardiac hypertrophy was associated with significantly enhanced contractile force at various concentrations of extracellular calcium and muscle lengths. Also, an amplified force-interval relationship in hypertrophied muscle at long rest intervals was found. However, this study revealed no change in calcium sensitivity of myofilaments. CONCLUSION: Altered intracellullar calcium handling contributes to enhanced contractile force in isoproterenol-induced cardiac hypertrophy.
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Tang et al. (1996) studied Isoproterenol-induced ventricular hypertrophy (rat heart). Isoproterenol was evaluated on Contractile force, calcium sensitivity of myofilaments, and force-interval relationship. Isoproterenol-induced cardiac hypertrophy in rats was associated with significantly enhanced contractile force driven by altered intracellular calcium handling, with no change in calcium sensitivity.
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