Intracellular Na$^+$ regulation in cardiac myocytes.
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Cardiovasc. Res. 57 (4): 897--912 (March 2003)

Intracellular Na$^+$ (Na$^+$i) is regulated in cardiac myocytes by a balance of Na$^+$ influx and efflux mechanisms. In the normal cell there is a large steady state electrochemical gradient favoring Na$^+$ influx. This potential energy is used by numerous transport mechanisms, including Na$^+$ channels and transporters which couple Na$^+$ influx to either co- or counter-transport of other ions and solutes. Six sarcolemmal Na$^+$ influx pathways are discussed in relatively quantitative terms: Na$^+$ channels, Na$^+$/Ca$^2+$ exchange, Na$^+$/H$^+$ exchange, Na$^+$/Mg2+ exchange, Na$^+$/HCO3- cotransport and Na$^+$/K$^+$/2Cl$^-$ cotransport. Under normal conditions Na$^+$/Ca$^2+$ exchange and Na$^+$ channels are the dominant Na$^+$ influx pathways, but other transporters may become increasingly important during altered conditions (e.g. acidosis or cell volume stress). Mitochondria also exhibit Na$^+$/Ca$^2+$ antiporter and Na$^+$/H$^+$ exchange activity that are important in mitochondrial function. These coupled fluxes of Na$^+$ with Ca$^2+$, H$^+$ and HCO3- make the detailed understanding of Na$^+$i regulation pivotal to the understanding of both cardiac excitation-contraction coupling and pH regulation. The Na$^+$/K$^+$-ATPase is the main route for Na$^+$ extrusion from cells and Na$^+$i is a primary regulator under physiological conditions. Na$^+$i is higher in rat than rabbit ventricular myocytes and the reason appears to be higher Na$^+$ influx in rat with a consequent rise in Na$^+$/K$^+$-ATPase activity (rather than lower Na$^+$/K$^+$-ATPase function in rat). This has direct functional consequences. There may also be subcellular Na$^+$i gradients locally in ventricular myocytes and this may also have important functional implications. Thus, the balance of Na$^+$ fluxes in heart cells may be complex, but myocyte Na$^+$ regulation is functionally important and merits focused attention as in this issue.
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