title: Role of the Renin-Angiotensin-Aldosterone System beyond Blood Pressure Regulation: Molecular and Cellular Mechanisms Involved in End-Organ Damage during Arterial Hypertension.
abstract: 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.
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Gen&#233;tica Molecular y Microbiolog&#237;a, Facultad de Ciencias Biol&#243;gicas, Pontificia Universidad Cat&#243;lica de Chile, 8330025 Santiago, Chile. nmunoz4@uc.cl.
authors.forename: Natalia
authors.initials: N
authors.lastname: Muñoz-Durango
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Endocrinolog&#237;a, Escuela de Medicina, Pontificia Universidad Cat&#243;lica de Chile, 8330074 Santiago, Chile. cristobal.fuentes.z@gmail.com.
authors.forename: Cristóbal A
authors.initials: CA
authors.lastname: Fuentes
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Endocrinolog&#237;a, Escuela de Medicina, Pontificia Universidad Cat&#243;lica de Chile, 8330074 Santiago, Chile. acastilloram@gmail.com.
authors.forename: Andrés E
authors.initials: AE
authors.lastname: Castillo
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Endocrinolog&#237;a, Escuela de Medicina, Pontificia Universidad Cat&#243;lica de Chile, 8330074 Santiago, Chile. luismartin.gonzalezgomez@gmail.com.
authors.forename: Luis Martín
authors.initials: LM
authors.lastname: González-Gómez
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Endocrinolog&#237;a, Escuela de Medicina, Pontificia Universidad Cat&#243;lica de Chile, 8330074 Santiago, Chile. andreavecchiola@gmail.com.
authors.forename: Andrea
authors.initials: A
authors.lastname: Vecchiola
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Endocrinolog&#237;a, Escuela de Medicina, Pontificia Universidad Cat&#243;lica de Chile, 8330074 Santiago, Chile. cfardella@med.puc.cl.
authors.forename: Carlos E
authors.initials: CE
authors.lastname: Fardella
authors.affiliation: Millenium Institute on Immunology and Immunotherapy, Departamento de Gen&#233;tica Molecular y Microbiolog&#237;a, Facultad de Ciencias Biol&#243;gicas, Pontificia Universidad Cat&#243;lica de Chile, 8330025 Santiago, Chile. akalergis@bio.puc.cl.|Millenium Institute on Immunology and Immunotherapy, Departamento de Endocrinolog&#237;a, Escuela de Medicina, Pontificia Universidad Cat&#243;lica de Chile, 8330074 Santiago, Chile. akalergis@bio.puc.cl.
authors.forename: Alexis M
authors.initials: AM
authors.lastname: Kalergis
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000378:metabolism / Q000473:pathology; D005355:Fibrosis; D006801:Humans; D006973:Hypertension / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000378:metabolism / Q000473:pathology; D012084:Renin-Angiotensin System
keywords: aldosterone; angiotensin II; end-organ damage; fibrosis; hypertension; primary aldosteronism; renin-angiotensin-aldosterone system (RAAS)