Zusammenfassung

The Na$^+$/Ca$^2+$ exchanger (NCX) is the main Ca$^2+$ 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 Ca$^2+$ current (I(Ca)) with an increase in ECC gain and (b) a shortening of the action potential (AP) to further limit Ca$^2+$ influx. Both mechanisms contribute to Ca$^2+$ homeostasis by reducing Ca$^2+$ influx while maintaining contractility. These adaptations may comprise important feedback mechanisms by which cardiomyocytes may be able to limit Ca$^2+$ influx in situations of compromised Ca$^2+$ extrusion capacity.

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The whole bibliography file I use.

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