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Authordc.contributor.authorHevia, Daniel 
Authordc.contributor.authorAraos, Patricio 
Authordc.contributor.authorPrado, Carolina 
Authordc.contributor.authorFuentes Luppichini, Eugenia 
Authordc.contributor.authorRojas, Macarena 
Authordc.contributor.authorAlzamora Miranda, Rodrigo 
Authordc.contributor.authorCifuentes Araneda, Flavia 
Authordc.contributor.authorGonzález, Alexis A. 
Authordc.contributor.authorAmador, Cristian A. 
Authordc.contributor.authorPacheco, Rodrigo 
Authordc.contributor.authorMichea Acevedo, Luis 
Admission datedc.date.accessioned2018-08-06T20:17:56Z
Available datedc.date.available2018-08-06T20:17:56Z
Publication datedc.date.issued2018
Cita de ítemdc.identifier.citationHypertension 71 (4): 709-718es_ES
Identifierdc.identifier.other10.1161/HYPERTENSIONAHA.117.10145
Identifierdc.identifier.urihttps://repositorio.uchile.cl/handle/2250/150679
Abstractdc.description.abstractIncreasing evidence shows that antigen-presenting cells (APCs) are involved in the development of inflammation associated to hypertension. However, the potential role of APCs in the modulation of renal sodium transport has not been addressed. We hypothesized that APCs participate in renal sodium transport and, thus, development of high blood pressure in response to angiotensin II plus a high-salt diet. Using transgenic mice that allow the ablation of CD11c(high) APCs, we studied renal sodium transport, the intrarenal renin-angiotensin system components, blood pressure, and cardiac/renal tissue damage in response to angiotensin II plus a high-salt diet. Strikingly, we found that APCs are required for the development of hypertension and that the ablation/restitution of APCs produces rapid changes in the blood pressure in mice with angiotensin II plus a high-salt diet. Moreover, APCs were necessary for the induction of intrarenal renin-angiotensin system components and affected the modulation of natriuresis and tubular sodium transporters. Consistent with the prevention of hypertension, the ablation of APCs also prevented cardiac hypertrophy and the induction of several indicators of renal and cardiac damage. Thus, our findings indicate a prominent role of APCs as modulators of blood pressure by mechanisms including renal sodium handling, with kinetics that suggest the involvement of tubular cell functions in addition to the modulation of inflammation and adaptive immune response.es_ES
Patrocinadordc.description.sponsorshipFONDECYT 1130550 1171869 1151423 1170093 CONICYT-Basal PFB-16 FONDECYT-Iniciacion 11121217 11150542 FONDECYT-Postdoctorado 3160383 CONICYT-Doctorado 21130762 21130482 Universidad Andres Bello DI-1224-16/R Iniciativa Cientifica Milenio of the Ministry of Economy, Development and Tourism (Chile) P09/016-F ICMes_ES
Lenguagedc.language.isoenes_ES
Publisherdc.publisherLippincott Williams & Wilkinses_ES
Sourcedc.sourceHypertensiones_ES
Keywordsdc.subjectAngiotensin IIes_ES
Keywordsdc.subjectAntigen presenting cellses_ES
Keywordsdc.subjectEpithelial sodium channeles_ES
Keywordsdc.subjectHypertensiones_ES
Keywordsdc.subjectInflammationes_ES
Títulodc.titleMyeloid CD11c (+) antigen-presenting cells ablation prevents hypertension in response to angiotensin II plus high salt dietes_ES
Document typedc.typeArtículo de revistaes_ES
dcterms.accessRightsdcterms.accessRightsAcceso a solo metadatoses_ES
Catalogueruchile.catalogadortjnes_ES
Indexationuchile.indexArtículo de publicación ISIes_ES


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