Cardiac excitation-contraction coupling in the absence of Na$^+$ - Ca$^2+$ exchange.
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Cell Calcium 34 (1): 19-26 (July 2003)

We investigate cardiac excitation-contraction coupling in the absence of sarcolemmal Na$^+$ - Ca$^2+$ exchange using NCX1 knock out mice. Knock out of NCX1 is embryonic lethal, and we measure Ca$^2+$ transients and contractions in heart tubes from embryos at day 9.5 post coitum. Immunoblot and electron microscopy both indicate that sarcoplasmic reticular membranes are diminished in the knock out (NCX(-/-)) heart tubes. Both Ni$^2+$ and nifedipine block excitation-contraction coupling in NCX-containing (NCX+) and NCX(-/-) heart tubes indicating an essential role for the L-type Ca$^2+$ current. Under basal conditions (1Hz stimulation), the NCX(-/-) heart tubes have normal Ca$^2+$ transients but are unable to maintain homeostasis when Ca$^2+$ fluxes are increased by various interventions (increased stimulation frequency, caffeine, isoproterenol). In each case, the NCX(-/-) heart tubes respond to the intervention in a more deleterious manner (increased diastolic Ca$^2+$, decreased Ca$^2+$ transient) than the NCX+ heart tubes. Expression of the sarcolemmal Ca$^2+$ pump was not upregulated. The sarcolemmal Ca$^2+$ pump, however, was able to compensate surprisingly well for the absence of Na$^+$ - Ca$^2+$ exchange under basal conditions.
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