| First Author | Reuter H | Year | 2003 |
| Journal | Cell Calcium | Volume | 34 |
| Issue | 1 | Pages | 19-26 |
| PubMed ID | 12767889 | Mgi Jnum | J:102710 |
| Mgi Id | MGI:3607962 | Doi | 10.1016/s0143-4160(03)00018-6 |
| Citation | Reuter H, et al. (2003) Cardiac excitation-contraction coupling in the absence of Na(+) - Ca2+ exchange. Cell Calcium 34(1):19-26 |
| abstractText | 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(+) |
