Cardiovascular Research

Cardiovascular Research 2003 57(4):897-912; doi:10.1016/S0008-6363(02)00656-9
© 2003 by European Society of Cardiology

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Copyright © 2003, European Society of Cardiology

Intracellular Na⁺ regulation in cardiac myocytes

Donald M Bers^a,*, William H Barry^b and Sanda Despa^a

^aDepartment of Physiology, Loyola University Chicago, Stritch School of Medicine, 2160 South First Avenue, Maywood, IL 60153, USA
^bDivision of Cardiology, University of Utah, Health Science Center, Salt Lake City, UT 84132, USA

^* Corresponding author. Tel.: +1-708-216-1018; fax: +1-708-216-6308. dbers{at}lumc.edu

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⁺/Ca²⁺ exchange, Na⁺/H⁺ exchange, Na⁺/Mg²⁺ exchange, Na⁺/HCO₃^– cotransport and Na⁺/K⁺/2Cl^– cotransport. Under normal conditions Na⁺/Ca²⁺ 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⁺/Ca²⁺ antiporter and Na⁺/H⁺ exchange activity that are important in mitochondrial function. These coupled fluxes of Na⁺ with Ca²⁺, 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.

KEYWORDS Myocytes; Na/Ca-exchanger; Na/H-exchanger; Na/K-pump; Na-channel

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Online ISSN 1755-3245 - Print ISSN 0008-6363

Copyright © 2008 European Society of Cardiology

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