Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress

Angiotensin II (Ang II) modulates vasomotor tone, cell growth, and extracellular matrix deposition. This study analyzed the effect of atorvastatin in the possible alterations induced by Ang II on structure and mechanics of mesenteric resistance arteries and the signaling mechanisms involved. Wistar...

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Autores: Briones, AM, Rodríguez-Criado, N, Hernanz, R, García-Redondo, AB, Rodrígues-Díez, RR, Alonso, MJ, Egido, J, Ruiz-Ortega, M, Salaices, M
Tipo de recurso: artículo
Fecha de publicación:2009
País:España
Institución:Universidad Rey Juan Carlos
Repositorio:BURJC-Digital. Repositorio Institucional de la Universidad Rey Juan Carlos
OAI Identifier:oai:burjcdigital.urjc.es:10115/3291
Acceso en línea:http://hdl.handle.net/10115/3291
Access Level:acceso abierto
Palabra clave:Biología y Biomedicina
2411.03 Fisiología Cardiovascular
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spelling Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stressBriones, AMRodríguez-Criado, NHernanz, RGarcía-Redondo, ABRodrígues-Díez, RRAlonso, MJEgido, JRuiz-Ortega, MSalaices, MBiología y Biomedicina2411.03 Fisiología CardiovascularAngiotensin II (Ang II) modulates vasomotor tone, cell growth, and extracellular matrix deposition. This study analyzed the effect of atorvastatin in the possible alterations induced by Ang II on structure and mechanics of mesenteric resistance arteries and the signaling mechanisms involved. Wistar rats were infused with Ang II (100 ng/kg per day, SC minipumps, 2 weeks) with or without atorvastatin (5 mg/kg per day). Ang II increased blood pressure and plasmatic malondialdehyde levels. Compared with controls, mesenteric resistance arteries from Ang II¿treated rats showed the following: (1) decreased lumen diameter; (2) increased wall/lumen; (3) decreased number of adventitial, smooth muscle, and endothelial cells; (4) increased stiffness; (5) increased collagen deposition; and (6) diminished fenestrae area and number in the internal elastic lamina. Atorvastatin did not alter blood pressure but reversed all of the structural and mechanical alterations of mesenteric arteries, including collagen and elastin alterations. In mesenteric resistance arteries, Ang II increased vascular O2.- production and diminished endothelial NO synthase and CuZn/superoxide dismutase but did not modify extracellular-superoxide dismutase expression. Atorvastatin improved plasmatic and vascular oxidative stress, normalized endothelial NO synthase and CuZn/superoxide dismutase expression, and increased extracellular superoxide dismutase expression, showing antioxidant properties. Atorvastatin also diminished extracellular signal¿ regulated kinase 1/2 activation caused by Ang II in these vessels, indicating an interaction with Ang II¿induced intracellular responses. In vascular smooth muscle cells, collagen type I release mediated by Ang II was reduced by different antioxidants and statins. Moreover, atorvastatin downregulated the Ang II¿induced NADPH oxidase subunit, Nox1, expression. Our results suggest that statins might exert beneficial effects on hypertension-induced vascular remodeling by improving vascular structure, extracellular matrix alterations, and vascular stiffness. These effects might be mediated by their antioxidant properties.Ciencias de la Salud III201020102009info:eu-repo/semantics/articleapplication/pdfhttp://hdl.handle.net/10115/3291reponame:BURJC-Digital. Repositorio Institucional de la Universidad Rey Juan Carlosinstname:Universidad Rey Juan CarlosInglésinfo:eu-repo/semantics/openAccessoai:burjcdigital.urjc.es:10115/32912026-06-24T12:48:17Z
dc.title.none.fl_str_mv Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
title Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
spellingShingle Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
Briones, AM
Biología y Biomedicina
2411.03 Fisiología Cardiovascular
title_short Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
title_full Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
title_fullStr Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
title_full_unstemmed Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
title_sort Atorvastatin prevents angiotensin II-induced vascular remodeling and oxidative stress
dc.creator.none.fl_str_mv Briones, AM
Rodríguez-Criado, N
Hernanz, R
García-Redondo, AB
Rodrígues-Díez, RR
Alonso, MJ
Egido, J
Ruiz-Ortega, M
Salaices, M
author Briones, AM
author_facet Briones, AM
Rodríguez-Criado, N
Hernanz, R
García-Redondo, AB
Rodrígues-Díez, RR
Alonso, MJ
Egido, J
Ruiz-Ortega, M
Salaices, M
author_role author
author2 Rodríguez-Criado, N
Hernanz, R
García-Redondo, AB
Rodrígues-Díez, RR
Alonso, MJ
Egido, J
Ruiz-Ortega, M
Salaices, M
author2_role author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Biología y Biomedicina
2411.03 Fisiología Cardiovascular
topic Biología y Biomedicina
2411.03 Fisiología Cardiovascular
description Angiotensin II (Ang II) modulates vasomotor tone, cell growth, and extracellular matrix deposition. This study analyzed the effect of atorvastatin in the possible alterations induced by Ang II on structure and mechanics of mesenteric resistance arteries and the signaling mechanisms involved. Wistar rats were infused with Ang II (100 ng/kg per day, SC minipumps, 2 weeks) with or without atorvastatin (5 mg/kg per day). Ang II increased blood pressure and plasmatic malondialdehyde levels. Compared with controls, mesenteric resistance arteries from Ang II¿treated rats showed the following: (1) decreased lumen diameter; (2) increased wall/lumen; (3) decreased number of adventitial, smooth muscle, and endothelial cells; (4) increased stiffness; (5) increased collagen deposition; and (6) diminished fenestrae area and number in the internal elastic lamina. Atorvastatin did not alter blood pressure but reversed all of the structural and mechanical alterations of mesenteric arteries, including collagen and elastin alterations. In mesenteric resistance arteries, Ang II increased vascular O2.- production and diminished endothelial NO synthase and CuZn/superoxide dismutase but did not modify extracellular-superoxide dismutase expression. Atorvastatin improved plasmatic and vascular oxidative stress, normalized endothelial NO synthase and CuZn/superoxide dismutase expression, and increased extracellular superoxide dismutase expression, showing antioxidant properties. Atorvastatin also diminished extracellular signal¿ regulated kinase 1/2 activation caused by Ang II in these vessels, indicating an interaction with Ang II¿induced intracellular responses. In vascular smooth muscle cells, collagen type I release mediated by Ang II was reduced by different antioxidants and statins. Moreover, atorvastatin downregulated the Ang II¿induced NADPH oxidase subunit, Nox1, expression. Our results suggest that statins might exert beneficial effects on hypertension-induced vascular remodeling by improving vascular structure, extracellular matrix alterations, and vascular stiffness. These effects might be mediated by their antioxidant properties.
publishDate 2009
dc.date.none.fl_str_mv 2009
2010
2010
dc.type.none.fl_str_mv info:eu-repo/semantics/article
format article
dc.identifier.none.fl_str_mv http://hdl.handle.net/10115/3291
url http://hdl.handle.net/10115/3291
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:BURJC-Digital. Repositorio Institucional de la Universidad Rey Juan Carlos
instname:Universidad Rey Juan Carlos
instname_str Universidad Rey Juan Carlos
reponame_str BURJC-Digital. Repositorio Institucional de la Universidad Rey Juan Carlos
collection BURJC-Digital. Repositorio Institucional de la Universidad Rey Juan Carlos
repository.name.fl_str_mv
repository.mail.fl_str_mv
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