Endogenous angiotensin II modulates nNOS expression in renovascular hypertension

dc.date.accessioned2011-03-15T20:01:11Z
dc.date.available2011-03-15T20:01:11Z
dc.identifier.citationPEREIRA, T. M. C. et al. Endogenous angiotensin II modulates nNOS expression in renovascular hypertension. Braz J Med Biol Res, Ribeirão Preto, v. 42, n. 7, p. 685-691, jul. 2009. Disponível em: <http://www.scielo.br/pdf/bjmbr/v42n7/7518.pdf>. Acesso em: 23 fev. 2011.por
dc.identifier.doi10.1590/S0100-879X2009000700014
dc.identifier.issn1678-4510
dc.identifier.urihttp://repositorio.ufes.br/handle/10/630
dc.rightsopen accessen
dc.titleEndogenous angiotensin II modulates nNOS expression in renovascular hypertensionpor
dc.typearticleen
dcterms.abstractNitric oxide (NO) influences renal blood flow mainly as a result of neuronal nitric oxide synthase (nNOS). Nevertheless, it is unclear how nNOS expression is modulated by endogenous angiotensin II, an inhibitor of NO function. We tested the hypothesis that the angiotensin II AT1 receptor and oxidative stress mediated by NADPH oxidase contribute to the modulation of renal nNOS expression in two-kidney, one-clip (2K1C) hypertensive rats. Experiments were performed on male Wistar rats (150 to 170 g body weight) divided into 2K1C (N = 19) and sham-operated (N = 19) groups. nNOS expression in kidneys of 2K1C hypertensive rats (N = 9) was compared by Western blotting to that of 2K1C rats treated with low doses of the AT1 antagonist losartan (10 mg·kg-1·day-1; N = 5) or the superoxide scavenger tempol (0.2 mmol·kg-1·day-1; N = 5), which still remain hypertensive. After 28 days, nNOS expression was significantly increased by 1.7-fold in the clipped kidneys of 2K1C rats and by 3-fold in the non-clipped kidneys of 2K1C rats compared with sham rats, but was normalized by losartan. With tempol treatment, nNOS expression increased 2-fold in the clipped kidneys and 1.4-fold in the non-clipped kidneys compared with sham rats. The changes in nNOS expression were not followed by changes in the enzyme activity, as measured indirectly by the cGMP method. In conclusion, AT1 receptors and oxidative stress seem to be primary stimuli for increased nNOS expression, but this up-regulation does not result in higher enzyme activity.eng
dcterms.creatorPereira, Thiago de Melo Costa
dcterms.creatorBalarini, Camille de Moura
dcterms.creatorSilva, Ian Victor
dcterms.creatorVasquez, Elisardo C. (Elisardo Corral)
dcterms.creatorMeyrelles, Silvana dos Santos
dcterms.issued2009-07
dcterms.languageengen
dcterms.subjectÓxido nítricopor
dcterms.subjectLosartanpor
dcterms.subjectHipertensão renovascularpor
dcterms.subjectLosartaneng
dcterms.subjectTempoleng
dcterms.subjectHypertension, Renovasculareng
dcterms.subjectNitric oxideeng
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