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Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System

Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and anim...

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Detalles Bibliográficos
Autor principal: Park, Jeanie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3420153/
https://www.ncbi.nlm.nih.gov/pubmed/22919537
http://dx.doi.org/10.1155/2012/319432
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author Park, Jeanie
author_facet Park, Jeanie
author_sort Park, Jeanie
collection PubMed
description Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications.
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spelling pubmed-34201532012-08-23 Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System Park, Jeanie Cardiol Res Pract Review Article Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications. Hindawi Publishing Corporation 2012 2012-08-07 /pmc/articles/PMC3420153/ /pubmed/22919537 http://dx.doi.org/10.1155/2012/319432 Text en Copyright © 2012 Jeanie Park. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Park, Jeanie
Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System
title Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System
title_full Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System
title_fullStr Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System
title_full_unstemmed Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System
title_short Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System
title_sort cardiovascular risk in chronic kidney disease: role of the sympathetic nervous system
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3420153/
https://www.ncbi.nlm.nih.gov/pubmed/22919537
http://dx.doi.org/10.1155/2012/319432
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