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
Digital Object Identifier (DOI)
https://doi.org/10.3389/fphys.2018.01303
Funding Information
This work was supported by NIH (Grant R01HL135000).
Repository Citation
Despa, Sanda, "Myocyte [Na+]i Dysregulation in Heart Failure and Diabetic Cardiomyopathy" (2018). Pharmacology and Nutritional Sciences Faculty Publications. 74.
https://uknowledge.uky.edu/pharmacol_facpub/74
Included in
Cardiovascular Diseases Commons, Cardiovascular System Commons, Endocrinology, Diabetes, and Metabolism Commons, Medical Cell Biology Commons, Medical Nutrition Commons, Medical Pharmacology Commons, Medical Physiology Commons, Pharmacology, Toxicology and Environmental Health Commons
Notes/Citation Information
Published in Frontiers in Physiology, v. 9, 1303, p. 1-8.
© 2018 Despa.
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