Role of the bradykinin B-2 receptor for the local and systemic inflammatory response that follows severe reperfusion injury

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dc.contributor.authorSouza, Daniele G.
dc.contributor.authorPinho, Vanessa
dc.contributor.authorPesquero, Jorge L.
dc.contributor.authorLomez, Eliane S.
dc.contributor.authorPoole, Steve
dc.contributor.authorJuliano, Luiz [UNIFESP]
dc.contributor.authorCorrea Junior, Ary
dc.contributor.authorCastro, M Salete D
dc.contributor.authorTeixeira, Mauro M.
dc.contributor.institutionUniversidade Federal de Minas Gerais (UFMG)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionNatl Inst Biol Stand & Controls
dc.date.accessioned2016-01-24T12:33:48Z
dc.date.available2016-01-24T12:33:48Z
dc.date.issued2003-05-01
dc.description.abstract1 Bradykinin (BK) appears to play an important role in the development and maintenance of inflammation. Here, we assessed the role of the BK B-2 receptor for the injuries that occur after ischemia and reperfusion (I/R) of the territory irrigated by the superior mesenteric artery.2 Tissue (lung and duodenum) kallikrein activity increased after ischemia with greater enhancement after reperfusion. A selective inhibitor of tissue kallikrein, Phenylacetyl-Phe-Ser-Arg-N-(2,3-dinitrophenyl)-ethylenediamine (TKI, 0.001 - 10 mg ml(-1)), inhibited kallikrein activity in a concentration-dependent manner in vitro. in vivo, pretreatment with TKI (30 mg kg(-1)) prevented the extravasation of plasma and the recruitment of neutrophils.3 Similarly, the bradykinin B-2 receptor antagonists, HOE 140 (0.01-1.0 mg kg(-1)) or FR173657 (10.0 mg kg(-1)), inhibited reperfusion-induced increases in vascular permeability and the recruitment of neutrophils in the intestine and lungs.4 in a model of more severe I/R injury, HOE 140 (1.0mg kg(-1)) inhibited the increase in vascular permeability, neutrophil recruitment, haemorrhage and tissue pathology. Furthermore, HOE 140 significantly inhibited the elevations of TNF-alpha in tissue and serum and partially prevented lethality. This was associated with an increase in the concentrations of IL-10 in tissue and serum.5 Thus, our results demonstrate that, following intestinal I/R injury, there is an increase in tissue kallikrein activity and activation of BK B-2 receptors. B-2 receptor activation is essential for the development of inflammatory tissue injury and lethality. These results contrast with those of others showing that BK mostly exerts a protective role during I/R injury.en
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Bioquim & Imunol, Belo Horizonte, MG, Brazil
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Farmacol, Belo Horizonte, MG, Brazil
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Microbiol, Belo Horizonte, MG, Brazil
dc.description.affiliationUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biofis, São Paulo, Brazil
dc.description.affiliationNatl Inst Biol Stand & Controls, Div Endocrinol, Potters Bar EN6 3QG, Herts, England
dc.description.affiliationUniv Fed Minas Gerais, Inst Ciencias Biol, Dept Fisiol & Biofis, Belo Horizonte, MG, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biofis, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent129-139
dc.identifierhttp://dx.doi.org/10.1038/sj.bjp.0705200
dc.identifier.citationBritish Journal of Pharmacology. London: Nature Publishing Group, v. 139, n. 1, p. 129-139, 2003.
dc.identifier.doi10.1038/sj.bjp.0705200
dc.identifier.issn0007-1188
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/27215
dc.identifier.wosWOS:000183125500015
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relation.ispartofBritish Journal of Pharmacology
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectischemia and reperfusionen
dc.subjectcytokinesen
dc.subjectTNF-alphaen
dc.subjectbradykininen
dc.subjectneutrophilsen
dc.subjectshocken
dc.titleRole of the bradykinin B-2 receptor for the local and systemic inflammatory response that follows severe reperfusion injuryen
dc.typeinfo:eu-repo/semantics/article
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