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Sodium Intake and Heart Failure

Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased my...

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Detalles Bibliográficos
Autores principales: Patel, Yash, Joseph, Jacob
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7763082/
https://www.ncbi.nlm.nih.gov/pubmed/33322108
http://dx.doi.org/10.3390/ijms21249474
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author Patel, Yash
Joseph, Jacob
author_facet Patel, Yash
Joseph, Jacob
author_sort Patel, Yash
collection PubMed
description Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.
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spelling pubmed-77630822020-12-27 Sodium Intake and Heart Failure Patel, Yash Joseph, Jacob Int J Mol Sci Review Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure. MDPI 2020-12-13 /pmc/articles/PMC7763082/ /pubmed/33322108 http://dx.doi.org/10.3390/ijms21249474 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Patel, Yash
Joseph, Jacob
Sodium Intake and Heart Failure
title Sodium Intake and Heart Failure
title_full Sodium Intake and Heart Failure
title_fullStr Sodium Intake and Heart Failure
title_full_unstemmed Sodium Intake and Heart Failure
title_short Sodium Intake and Heart Failure
title_sort sodium intake and heart failure
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7763082/
https://www.ncbi.nlm.nih.gov/pubmed/33322108
http://dx.doi.org/10.3390/ijms21249474
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