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PPARs in the Renal Regulation of Systemic Blood Pressure

Recent research has revealed roles for the peroxisome proliferator activated receptor (PPAR) family of transcription factors in blood pressure regulation, expanding the possible therapeutic use of PPAR ligands. PPARα and PPARγ modulate the renin-angiotensin-aldosterone system (RAAS), a major regulat...

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Detalles Bibliográficos
Autores principales: Rőszer, Tamás, Ricote, Mercedes
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896854/
https://www.ncbi.nlm.nih.gov/pubmed/20613959
http://dx.doi.org/10.1155/2010/698730
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author Rőszer, Tamás
Ricote, Mercedes
author_facet Rőszer, Tamás
Ricote, Mercedes
author_sort Rőszer, Tamás
collection PubMed
description Recent research has revealed roles for the peroxisome proliferator activated receptor (PPAR) family of transcription factors in blood pressure regulation, expanding the possible therapeutic use of PPAR ligands. PPARα and PPARγ modulate the renin-angiotensin-aldosterone system (RAAS), a major regulator of systemic blood pressure and interstitial fluid volume by transcriptional control of renin, angiotensinogen, angiotensin converting enzyme (ACE) and angiotensin II receptor 1 (AT-R1). Blockade of RAAS is an important therapeutic target in hypertension management and attenuates microvascular damage, glomerular inflammation and left ventricular hypertrophy in hypertensive patients and also show antidiabetic effects. The mechanisms underlying the benefits of RAAS inhibition appear to involve PPARγ-regulated pathways. This review summarizes current knowledge on the role of PPARs in the transcriptional control of the RAAS and the possible use of PPAR ligands in the treatment of RAAS dependent hypertension.
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spelling pubmed-28968542010-07-07 PPARs in the Renal Regulation of Systemic Blood Pressure Rőszer, Tamás Ricote, Mercedes PPAR Res Review Article Recent research has revealed roles for the peroxisome proliferator activated receptor (PPAR) family of transcription factors in blood pressure regulation, expanding the possible therapeutic use of PPAR ligands. PPARα and PPARγ modulate the renin-angiotensin-aldosterone system (RAAS), a major regulator of systemic blood pressure and interstitial fluid volume by transcriptional control of renin, angiotensinogen, angiotensin converting enzyme (ACE) and angiotensin II receptor 1 (AT-R1). Blockade of RAAS is an important therapeutic target in hypertension management and attenuates microvascular damage, glomerular inflammation and left ventricular hypertrophy in hypertensive patients and also show antidiabetic effects. The mechanisms underlying the benefits of RAAS inhibition appear to involve PPARγ-regulated pathways. This review summarizes current knowledge on the role of PPARs in the transcriptional control of the RAAS and the possible use of PPAR ligands in the treatment of RAAS dependent hypertension. Hindawi Publishing Corporation 2010 2010-06-08 /pmc/articles/PMC2896854/ /pubmed/20613959 http://dx.doi.org/10.1155/2010/698730 Text en Copyright © 2010 T. Rőszer and M. Ricote. 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
Rőszer, Tamás
Ricote, Mercedes
PPARs in the Renal Regulation of Systemic Blood Pressure
title PPARs in the Renal Regulation of Systemic Blood Pressure
title_full PPARs in the Renal Regulation of Systemic Blood Pressure
title_fullStr PPARs in the Renal Regulation of Systemic Blood Pressure
title_full_unstemmed PPARs in the Renal Regulation of Systemic Blood Pressure
title_short PPARs in the Renal Regulation of Systemic Blood Pressure
title_sort ppars in the renal regulation of systemic blood pressure
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896854/
https://www.ncbi.nlm.nih.gov/pubmed/20613959
http://dx.doi.org/10.1155/2010/698730
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