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Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension

Arterial hypertension is a common condition worldwide and an important predictor of several complicated diseases. Arterial hypertension can be triggered by many factors, including physiological, genetic, and lifestyle causes. Specifically, molecules of the renin-angiotensin-aldosterone system not on...

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Autores principales: Muñoz-Durango, Natalia, Fuentes, Cristóbal A., Castillo, Andrés E., González-Gómez, Luis Martín, Vecchiola, Andrea, Fardella, Carlos E., Kalergis, Alexis M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964362/
https://www.ncbi.nlm.nih.gov/pubmed/27347925
http://dx.doi.org/10.3390/ijms17070797
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author Muñoz-Durango, Natalia
Fuentes, Cristóbal A.
Castillo, Andrés E.
González-Gómez, Luis Martín
Vecchiola, Andrea
Fardella, Carlos E.
Kalergis, Alexis M.
author_facet Muñoz-Durango, Natalia
Fuentes, Cristóbal A.
Castillo, Andrés E.
González-Gómez, Luis Martín
Vecchiola, Andrea
Fardella, Carlos E.
Kalergis, Alexis M.
author_sort Muñoz-Durango, Natalia
collection PubMed
description Arterial hypertension is a common condition worldwide and an important predictor of several complicated diseases. Arterial hypertension can be triggered by many factors, including physiological, genetic, and lifestyle causes. Specifically, molecules of the renin-angiotensin-aldosterone system not only play important roles in the control of blood pressure, but they are also associated with the genesis of arterial hypertension, thus constituting a need for pharmacological interventions. Chronic high pressure generates mechanical damage along the vascular system, heart, and kidneys, which are the principal organs affected in this condition. In addition to mechanical stress, hypertension-induced oxidative stress, chronic inflammation, and the activation of reparative mechanisms lead to end-organ damage, mainly due to fibrosis. Clinical trials have demonstrated that renin-angiotensin-aldosterone system intervention in hypertensive patients lowers morbidity/mortality and inflammatory marker levels as compared to placebo patients, evidencing that this system controls more than blood pressure. This review emphasizes the detrimental effects that a renin-angiotensin-aldosterone system (RAAS) imbalance has on health considerations above and beyond high blood pressure, such as fibrotic end-organ damage.
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spelling pubmed-49643622016-08-03 Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension Muñoz-Durango, Natalia Fuentes, Cristóbal A. Castillo, Andrés E. González-Gómez, Luis Martín Vecchiola, Andrea Fardella, Carlos E. Kalergis, Alexis M. Int J Mol Sci Review Arterial hypertension is a common condition worldwide and an important predictor of several complicated diseases. Arterial hypertension can be triggered by many factors, including physiological, genetic, and lifestyle causes. Specifically, molecules of the renin-angiotensin-aldosterone system not only play important roles in the control of blood pressure, but they are also associated with the genesis of arterial hypertension, thus constituting a need for pharmacological interventions. Chronic high pressure generates mechanical damage along the vascular system, heart, and kidneys, which are the principal organs affected in this condition. In addition to mechanical stress, hypertension-induced oxidative stress, chronic inflammation, and the activation of reparative mechanisms lead to end-organ damage, mainly due to fibrosis. Clinical trials have demonstrated that renin-angiotensin-aldosterone system intervention in hypertensive patients lowers morbidity/mortality and inflammatory marker levels as compared to placebo patients, evidencing that this system controls more than blood pressure. This review emphasizes the detrimental effects that a renin-angiotensin-aldosterone system (RAAS) imbalance has on health considerations above and beyond high blood pressure, such as fibrotic end-organ damage. MDPI 2016-06-23 /pmc/articles/PMC4964362/ /pubmed/27347925 http://dx.doi.org/10.3390/ijms17070797 Text en © 2016 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
Muñoz-Durango, Natalia
Fuentes, Cristóbal A.
Castillo, Andrés E.
González-Gómez, Luis Martín
Vecchiola, Andrea
Fardella, Carlos E.
Kalergis, Alexis M.
Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension
title Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension
title_full Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension
title_fullStr Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension
title_full_unstemmed Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension
title_short Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension
title_sort role of the renin-angiotensin-aldosterone system beyond blood pressure regulation: molecular and cellular mechanisms involved in end-organ damage during arterial hypertension
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4964362/
https://www.ncbi.nlm.nih.gov/pubmed/27347925
http://dx.doi.org/10.3390/ijms17070797
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