In rabbit ventricular cells, the skeletal Na+ channel isoform (Nav1.4) is the main isoform responsible for priming the dyadic cleft via reverse Na+-Ca2+ exchanger activation.
The skeletal Na+ channel isoform Nav1.4 is primarily responsible for priming the dyadic cleft via reverse NCX, which may be relevant in remodeled excitation-contraction coupling.
A number of studies suggest that the Na + -Ca 2+ exchanger (NCX) activated by Na + currents is involved in the process of excitation-contraction (EC) coupling in cardiac ventricular myocytes. Although insufficient to trigger sarcoplasmic Ca 2+ release alone, the Ca 2+ entering through reverse NCX during an action potential can prime the dyadic cleft and increase the Ca 2+ current coupling fidelity. Using specific Na + inhibitors in this study, we show that in rabbit ventricular cells the skeletal Na + channel isoform (Na v 1.4) is the main isoform responsible for this priming. Our study provides insights into a mechanism that may have an increased relevance where EC coupling is remodeled.
Natalia S. Torres (Fri,) reported a other. Specific Na+ inhibitors was evaluated on Role of skeletal Na+ channel isoform (Nav1.4) in priming the dyadic cleft. In rabbit ventricular cells, the skeletal Na+ channel isoform (Nav1.4) is the main isoform responsible for priming the dyadic cleft via reverse Na+-Ca2+ exchanger activation.
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