Na+ transport in the normal and failing heart - Remember the balance

Sanda Despa, Donald M. Bers

Research output: Contribution to journalReview articlepeer-review

108 Scopus citations


In the heart, intracellular Na+ concentration ([Na+]i) is a key modulator of Ca2+ 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+/Ca2+ 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.".

Original languageEnglish
Pages (from-to)2-10
Number of pages9
JournalJournal of Molecular and Cellular Cardiology
StatePublished - Aug 2013

Bibliographical note

Funding Information:
This work was supported in part by NIH (grants HL-109501 to SD; HL-81526 to DMB).


  • Heart failure
  • Intracellular Na concentration
  • Myocyte
  • Na/Ca exchanger
  • Na/H exchanger
  • Na/K-ATPase

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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