Genetic manipulation of cardiac Na$^+$/Ca$^2+$ exchange expression.
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Biochem. Biophys. Res. Commun. 322 (4): 1336--1340 (October 2004)

The Na$^+$/Ca$^2+$ exchanger (NCX) is the primary Ca$^2+$ extrusion mechanism in cardiomyocytes. To further investigate the role of NCX in excitation-contraction coupling and Ca$^2+$ homeostasis, we created murine models with altered expression levels of NCX. Homozygous overexpression of NCX resulted in mild cardiac hypertrophy. Decline of the Ca$^2+$ transient and relaxation of contraction were increased and the reverse mode of NCX was augmented. Overexpression also led to a higher susceptibility to ischemia-reperfusion injury and to a greater ability of NCX to trigger Ca$^2+$-induced Ca$^2+$ release. Furthermore, an increase in peak L-type Ca$^2+$ current was observed suggesting a direct influence of NCX on L-type Ca$^2+$ current. Whereas global knockout of NCX led to prenatal death, a recently generated cardiac-specific NCX knockout mouse was viable with surprisingly normal contractile properties. Expression levels of other Ca$^2+$-handling proteins were not altered. Ca$^2+$ influx in these animals is limited by a decrease of peak L-type Ca$^2+$ current. An alternative Ca$^2+$ efflux mechanism, presumably the plasma membrane Ca$^2+$-ATPase, is sufficient to maintain Ca$^2+$-homeostasis in the NCX knockout mice.
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