Inhibition of central angiotensin II-induced pressor responses by hydrogen peroxide.

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dc.contributor.authorLauar, M. R.
dc.contributor.authorColombari, Débora Simões de Almeida
dc.contributor.authorPaula, Patricia Maria de
dc.contributor.authorColombari, Eduardo
dc.contributor.authorCardoso, Leonardo Máximo
dc.contributor.authorLuca Junior, L. A. de
dc.contributor.authorMenani, José Vanderlei
dc.date.accessioned2015-03-03T16:45:01Z
dc.date.available2015-03-03T16:45:01Z
dc.date.issued2010
dc.description.abstractHydrogen peroxide (H2O2), important reactive oxygen species produced endogenously, may have different physiological actions. The superoxide anion (O2 •_) is suggested to be part of the signaling mechanisms activated by angiotensin II (ANG II) and central virus-mediated overexpression of the enzyme superoxide dismutase (that dismutates O2 •_ to H2O2) reduces pressor and dipsogenic responses to central ANG II. Whether this result might reflect elevation of H2O2 rather than depletion of O2 •_ has not been addressed. Here we investigated the effects of H2O2 injected intracerebroventricularly (i.c.v.) or ATZ (3-amino-1,2,4-triazole, a catalase inhibitor) injected intravenously (i.v.) or i.c.v. on the pressor responses induced by i.c.v. injections of ANG II. Normotensive male Holtzman rats (280–320 g, n_5–13/ group) with stainless steel cannulas implanted in the lateral ventricle were used. Prior injection of H2O2 (5 _mol/1 _l) or ATZ (5 nmol/1 _l) i.c.v. almost abolished the pressor responses induced by ANG II (50 ng/1 _l) also injected i.c.v. (7_3 and 5_3 mm Hg, respectively, vs. control: 19_4 mm Hg). Injection of ATZ (3.6 mmol/kg b.wt.) i.v. also reduced central ANG II-induced pressor responses. Injections of H2O2 i.c.v. and ATZ i.c.v. or i.v. alone produced no effect on baseline arterial pressure. Central ANG II, H2O2 or ATZ did not affect heart rate. The results show that central injections of H2O2 and central or peripheral injections of ATZ reduced the pressor responses induced by i.c.v. ANG II, suggesting that exogenous or endogenous H2O2 may inhibit central pressor mechanisms activated by ANG II.pt_BR
dc.identifier.citationLAUAR, M . R. et al. Inhibition of central angiotensin II-induced pressor responses by hydrogen peroxide. Neuroscience, v. 171, p. 524-530, 2010. Disponível em: <http://www.sciencedirect.com/science/article/pii/S0306452210011760>. Acesso em: 08 nov. 2014.pt_BR
dc.identifier.doihttps://doi.org/10.1016/j.neuroscience.2010.08.048
dc.identifier.issn0306-4522
dc.identifier.urihttp://www.repositorio.ufop.br/handle/123456789/4526
dc.language.isoen_USpt_BR
dc.rights.licenseO periódico Neuroscience concede permissão para depósito deste artigo no Repositório Institucional da UFOP. Número da licença: 3525480449766.pt_BR
dc.subjectHypertensionpt_BR
dc.subjectReactive oxygen speciespt_BR
dc.subjectSuperoxide dismutasept_BR
dc.subjectArterial pressurept_BR
dc.subjectCatalase inhibitorpt_BR
dc.titleInhibition of central angiotensin II-induced pressor responses by hydrogen peroxide.pt_BR
dc.typeArtigo publicado em periodicopt_BR
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