Na+ transport in the normal and failing heart—remember the balance

S Despa, DM Bers - Journal of molecular and cellular cardiology, 2013 - Elsevier
S Despa, DM Bers
Journal of molecular and cellular cardiology, 2013Elsevier
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 …
Abstract
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."
Elsevier