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dc.contributor.authorBlanch, Graziela Torres [UNESP]
dc.contributor.authorFreiria-Oliveira, Andre Henrique [UNESP]
dc.contributor.authorFina Speretta, Guilherme Fleury [UNESP]
dc.contributor.authorCarrera, Eduardo J.
dc.contributor.authorLi, Hongwei
dc.contributor.authorSpeth, Robert C.
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.authorSumners, Colin
dc.contributor.authorColombari, Debora S. A. [UNESP]
dc.date.accessioned2015-03-18T15:55:39Z
dc.date.available2015-03-18T15:55:39Z
dc.date.issued2014-10-01
dc.identifierhttp://dx.doi.org/10.1161/HYPERTENSIONAHA.114.03188
dc.identifier.citationHypertension. Philadelphia: Lippincott Williams & Wilkins, v. 64, n. 4, p. 777-+, 2014.
dc.identifier.issn0194-911X
dc.identifier.urihttp://hdl.handle.net/11449/117259
dc.description.abstractAngiotensin II increases and decreases arterial pressure by acting at angiotensin type 1 and type 2 receptors, respectively. Renovascular hypertensive rats exhibit a high level of activity of the peripheral and central renin-angiotensin system. Therefore, in the present study, we evaluated the effect of increasing the expression of angiotensin type 2 receptors in the solitary-vagal complex (nucleus of the solitary tract/dorsal motor nucleus of the vagus), a key brain stem region for cardiovascular regulation, on the development of renovascular hypertension. Holtzman normotensive rats were implanted with a silver clip around the left renal artery to induce 2-kidney 1-clip renovascular hypertension. Three weeks later, rats were microinjected in the solitary-vagal complex with either an adenoassociated virus to increase the expression of angiotensin type 2 receptors or with a control vector. We observed that increasing angiotensin type 2 receptor expression in the solitary-vagal complex attenuated the development of renovascular hypertension and also reversed the impairment of the baroreflex and the increase in the low-frequency component of systolic blood pressure observed in renovascular hypertensive rats. Furthermore, an observed decrease in mRNA levels of angiotensin-converting enzyme 2 in the solitary-vagal complex of renovascular hypertensive rats was restored to control levels after viral-mediated increases in angiotensin type 2 receptors at this site. Collectively, these data demonstrate specific and beneficial effects of angiotensin type 2 receptors via the brain of hypertensive rats and suggest that central angiotensin type 2 receptors may be a potential target for therapeutics in renovascular hypertension.en
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorshipNational Institutes of Health
dc.format.extent777-+
dc.language.isoeng
dc.publisherLippincott Williams & Wilkins
dc.relation.ispartofHypertension
dc.sourceWeb of Science
dc.subjectangiotensin IIen
dc.subjectangiotensin-converting enzyme 2en
dc.subjectangiotensin receptor blockersen
dc.subjectbaroreflexen
dc.titleIncreased Expression of Angiotensin II Type 2 Receptors in the Solitary-Vagal Complex Blunts Renovascular Hypertensionen
dc.typeArtigo
dcterms.rightsHolderLippincott Williams & Wilkins
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionNova SE Univ
dc.contributor.institutionSouthern Med Univ
dc.contributor.institutionUniv Florida
dc.description.affiliationSao Paulo State Univ, Sch Dent, Dept Physiol & Pathol, Sao Paulo, Brazil
dc.description.affiliationNova SE Univ, Coll Pharm, Dept Pharmaceut Sci, Ft Lauderdale, FL 33314 USA
dc.description.affiliationSouthern Med Univ, Sch Biotechnol, Guangzhou, Guangdong, Peoples R China
dc.description.affiliationUniv Florida, Coll Med, Dept Physiol & Funct Genom, Gainesville, FL USA
dc.description.affiliationUniv Florida, Coll Med, McKnight Brain Inst, Gainesville, FL USA
dc.description.affiliationUnespSao Paulo State Univ, Sch Dent, Dept Physiol & Pathol, Sao Paulo, Brazil
dc.identifier.doi10.1161/HYPERTENSIONAHA.114.03188
dc.identifier.wosWOS:000341988000016
dc.rights.accessRightsAcesso restrito
dc.description.sponsorshipIdCNPq: 304918/2011-3
dc.description.sponsorshipIdCNPq: 473108/2011-9
dc.description.sponsorshipIdFAPESP: 11/50770-1
dc.description.sponsorshipIdFAPESP: 13/50121-9
dc.description.sponsorshipIdCAPES: PNPD/CAPES 2748/2010
dc.description.sponsorshipIdNational Institutes of HealthR01 HL076803
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt
dc.identifier.lattes4544450092427426
unesp.author.lattes4544450092427426[7]
unesp.author.orcid0000-0002-1395-4036[7]
dc.relation.ispartofjcr6.823
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