Chronic Antioxidant Treatment Improves Arterial Renovascular Hypertension and Oxidative Stress Markers in the Kidney in Wistar Rats

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dc.contributor.author Nishi, Erika Emy [UNIFESP]
dc.contributor.author Oliveira-Sales, Elizabeth Barbosa [UNIFESP]
dc.contributor.author Bergamaschi, Cassia T. [UNIFESP]
dc.contributor.author Cesar Oliveira, Thais Galvao [UNIFESP]
dc.contributor.author Boim, Mirian A. [UNIFESP]
dc.contributor.author Campos, Ruy R. [UNIFESP]
dc.date.accessioned 2016-01-24T13:59:39Z
dc.date.available 2016-01-24T13:59:39Z
dc.date.issued 2010-05-01
dc.identifier http://dx.doi.org/10.1038/ajh.2010.11
dc.identifier.citation American Journal of Hypertension. New York: Nature Publishing Group, v. 23, n. 5, p. 473-480, 2010.
dc.identifier.issn 0895-7061
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/32525
dc.description.abstract BACKGROUNDSympathetic vasomotor hyperactivity and baroreflex dysfunction are involved in the development and maintenance of renovascular arterial hypertension. We hypothesized that angiotensin (Ang) II-dependent oxidative stress contributes to the pathophysiology of the two-kidney, one-clip (2K-1C) model.METHODSThe mean arterial pressure (MAP), baroreflex, and renal sympathetic nerve activity (rSNA) were evaluated after chronic administration of an antioxidant, vitamin C (vitC 150 mg/kg/day) in male Wistar 2K-1C rats. Additionally, the mRNA levels of Ang II subtype 1 receptor (AT(1)R), NAD(P)H oxidase subunits (p47phox and gp91phox), and major antioxidant enzymes were evaluated in the renal cortex.RESULTSAfter vitC treatment, the MAP (170 +/- 4 vs. 133 +/- 6 mm Hg; P < 0.05) and rSNA (161 +/- 5 vs. 118 +/- 12 spikes/s; P < 0.05) were significantly reduced only in the 2K-1C group. VitC improved the baroreflex control of heart rate (HR) and rSNA. the expression of AT(1)R, p47phox, and gp91phox was elevated (51, 184, and 132%, respectively) in the clipped kidney of 2K-1C group. VitC downregulated AT(1)R in the clipped kidney (31%). Catalase (CAT) expression was reduced in clipped (70%) and nonclipped (83%) kidneys of 2K-1C rats. VitC treatment augmented the expression of glutathione peroxidase (GPx) in both clipped (185%) and nonclipped (212%) kidneys of the 2K-1C group.CONCLUSIONSThe present study suggests a role for oxidative stress in the cardiovascular and sympathetic alterations in renovascular hypertension, associated with changes in the expression of AT,R, NAD(P)H oxidase subunits, and antioxidant enzymes in the kidney. en
dc.description.sponsorship Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent 473-480
dc.language.iso eng
dc.publisher Nature Publishing Group
dc.relation.ispartof American Journal of Hypertension
dc.rights Acesso restrito
dc.subject baroreceptor reflex en
dc.subject blood pressure en
dc.subject hypertension en
dc.subject oxidative stress en
dc.subject renovascular en
dc.subject sympathetic nerve activity en
dc.subject vitamins en
dc.title Chronic Antioxidant Treatment Improves Arterial Renovascular Hypertension and Oxidative Stress Markers in the Kidney in Wistar Rats en
dc.type Artigo
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Universidade Federal de São Paulo, Dept Physiol, Div Cardiovasc, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo Baixada Santista, Dept Biosci, São Paulo, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Med, Div Nephrol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Physiol, Div Cardiovasc, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo Baixada Santista, Dept Biosci, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Med, Div Nephrol, São Paulo, Brazil
dc.description.sponsorshipID FAPESP: 04/15969-8
dc.description.sponsorshipID FAPESP: 06/59047-2
dc.description.sponsorshipID FAPESP: 07/56925-1
dc.identifier.doi 10.1038/ajh.2010.11
dc.description.source Web of Science
dc.identifier.wos WOS:000277162600010



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