Na(+)--Ca2+ exchange in the regulation of cardiac excitation-contraction coupling.

摘要: Cardiac sarcolemmal Na+–Ca2+ exchange is a central component of Ca2+ signaling essential for extrusion and contributing to variable degree the development systolic transient. Reports on differential gene expression in cardiac disease regulation its thermodynamic equilibrium depending intracellular gradients ion concentrations between subcellular compartments have recently put new complexion implications excitation–contraction (E–C) coupling. Heart failure models genetic approaches regulate exchanger improved our knowledge function. Modest overexpression heterozygous transgenic mice had minimal effects E–C coupling However, higher levels homozygotes led pathological hypertrophy with an increased interaction L-type current reduced gain. These results suggested that capable modulating sarcoplasmic handling at high may interact gating kinetics by means regulating subsarcolemmal levels. Despite being coupling, newly generated mouse model cardiac-specific conditional knock-out viable unchanged dynamics adult ventricular myocytes. myocytes adapt well exchanger, apparently reducing transsarcolemmal fluxes increasing gain possibly mediated changes submembrane For murine model, which relies primarily regulation, this suggestion role should be thought as buffering function not major transporter competition reticulum.