Abstract

By controlling the function of various sarcolemmal and mitochondrial ion transporters, intracellular Na+ concentration ([Na+]i) regulates Ca2+ cycling, electrical activity, the matching of energy supply and demand, and oxidative stress in cardiac myocytes. Thus, maintenance of myocyte Na+ homeostasis is vital for preserving the electrical and contractile activity of the heart. [Na+]i is set by the balance between the passive Na+ entry through numerous pathways and the pumping of Na+ out of the cell by the Na+/K+-ATPase. This equilibrium is perturbed in heart failure, resulting in higher [Na+]i. More recent studies have revealed that [Na+]i is also increased in myocytes from diabetic hearts. Elevated [Na+]i causes oxidative stress and augments the sarcoplasmic reticulum Ca2+ leak, thus amplifying the risk for arrhythmias and promoting heart dysfunction. This mini-review compares and contrasts the alterations in Na+ extrusion and/or Na+ uptake that underlie the [Na+]i increase in heart failure and diabetes, with a particular emphasis on the emerging role of Na+ - glucose cotransporters in the diabetic heart.

Document Type

Review

Publication Date

9-12-2018

Notes/Citation Information

Published in Frontiers in Physiology, v. 9, 1303, p. 1-8.

© 2018 Despa.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

Digital Object Identifier (DOI)

https://doi.org/10.3389/fphys.2018.01303

Funding Information

This work was supported by NIH (Grant R01HL135000).

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