Na: Plasticity of Cardiac Excitation–Contraction Coupling+: Plasticity of Cardiac Excitation–Contraction Coupling/Ca: Plasticity of Cardiac Excitation–Contraction Coupling2+: Plasticity of Cardiac Excitation–Contraction Coupling Exchanger Knockout Mice: Plasticity of Cardiac Excitation–Contraction Coupling

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Abstract

ABSTRACT

The Na+/Ca2+ exchanger (NCX) is the main Ca2+ extrusion mechanism of the cardiac myocyte. Nevertheless, cardiac-specific NCX knockout (KO) mice are viable to adulthood. We have identified two adaptations of excitation–contraction coupling (ECC) to the absence of NCX in these animals: (a) a reduction of the L-type Ca2+ current (ICa) with an increase in ECC gain and (b) a shortening of the action potential (AP) to further limit Ca2+ influx. Both mechanisms contribute to Ca2+ homeostasis by reducing Ca2+ influx while maintaining contractility. These adaptations may comprise important feedback mechanisms by which cardiomyocytes may be able to limit Ca2+ influx in situations of compromised Ca2+ extrusion capacity.

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