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J Mol Cell Cardiol. 2013 Aug;61:2-10. doi: 10.1016/j.yjmcc.2013.04.011. Epub 2013 Apr 19.

Na⁺ transport in the normal and failing heart - remember the balance.

Author information

1
Department of Pharmacology, University of California, Davis, CA, USA. sdespa@ucdavis.edu

Abstract

In the heart, intracellular Na(+) concentration ([Na(+)]i) is a key modulator of Ca(2+) cycling, contractility and cardiac myocyte metabolism. Several Na(+) transporters are electrogenic, thus they both contribute to shaping the cardiac action potential and at the same time are affected by it. [Na(+)]i is controlled by the balance between Na(+) influx through various pathways, including the Na(+)/Ca(2+) exchanger and Na(+) channels, and Na(+) extrusion via the Na(+)/K(+)-ATPase. [Na(+)]i is elevated in HF due to a combination of increased entry through Na(+) channels and/or Na(+)/H(+) exchanger and reduced activity of the Na(+)/K(+)-ATPase. Here we review the major Na(+) transport pathways in cardiac myocytes and how they participate in regulating [Na(+)]i in normal and failing hearts. This article is part of a Special Issue entitled "Na(+) Regulation in Cardiac Myocytes."

KEYWORDS:

AP; Ca(2+)/calmodulin dependent kinase II; CaMKII; DAD; FXYD; Heart failure; Intracellular Na(+) concentration; Myocyte; NBC; NCX; NHE; NKA; Na(+)/Ca(2+) exchanger; Na(+)/H(+) exchanger; Na(+)/HCO(3)(−) cotransporter; Na(+)/K(+)-ATPase; PLM; RyR; SR; TM; [Ca(2+)](i); [Ca(2+)](m); [Na(+)](i); action potential; concentration of free Ca(2+) in the cytosol; concentration of free Ca(2+) in the mitochondrial matrix; delayed afterdepolarization; family of proteins that are specific Na/K-ATPase regulators; intracellular Na(+) concentration; phospholemman; ryanodine receptor; sarcoplasmic reticulum; transmembrane domain

PMID:
23608603
PMCID:
PMC3720717
DOI:
10.1016/j.yjmcc.2013.04.011
[Indexed for MEDLINE]
Free PMC Article

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