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Cardiac hypertrophy is a growth response of the heart to increased hemodynamic demand or damage. Accompanying this heart enlargement is a remodeling of Ca²⁺ signaling. Due to its fundamental role in controlling cardiomyocyte contraction during every heartbeat, modifications in Ca²⁺ fluxes significantly impact on cardiac output and facilitate the development of arrhythmias. Using cardiomyocytes from spontaneously hypertensive rats (SHRs), we demonstrate that an increase in Ca²⁺ release through inositol 1,4,5-trisphosphate receptors (InsP₃Rs) contributes to the larger excitation contraction coupling (ECC)-mediated Ca²⁺ transients characteristic of hypertrophic myocytes and underlies the more potent enhancement of ECC-mediated Ca²⁺ transients and contraction elicited by InsP₃ or endothelin-1 (ET-1). Responsible for this is an increase in InsP₃R expression in the junctional sarcoplasmic reticulum …