The use of kinin B-1 and B-2 receptor knockout mice and selective antagonists to characterize the nociceptive responses caused by kinins at the spinal level

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dc.contributor.author Ferreira, J.
dc.contributor.author Campos, M. M.
dc.contributor.author Araujo, R.
dc.contributor.author Bader, M.
dc.contributor.author Pesquero, J. B.
dc.contributor.author Calixto, J. B.
dc.date.accessioned 2016-01-24T12:33:37Z
dc.date.available 2016-01-24T12:33:37Z
dc.date.issued 2002-12-01
dc.identifier http://dx.doi.org/10.1016/S0028-3908(02)00311-8
dc.identifier.citation Neuropharmacology. Oxford: Pergamon-Elsevier B.V., v. 43, n. 7, p. 1188-1197, 2002.
dc.identifier.issn 0028-3908
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/27059
dc.description.abstract The mechanisms by which kinins induce hyperalgesia in the spinal cord were investigated by using B-1 or B-2 knockout mice in conjunction with kinin selective agonists and antagonists. the i.t. administration of the kinin B-2 receptor agonists bradykinin (BK) or Tyr(8)-BK produced dose-related thermal hyperalgesia evaluated in the hot-plate test. BK-induced hyperalgesia was abolished by the beta(2) receptor antagonist Hoe 140. the i.t. injection of the kinin beta(1) receptor agonists, des-Arg(9)-bradykinin (DABK) or des-Arg(10)-okallidin (DAKD) also caused dose-related thermal hyperalgesia. Different from the beta(2) agonists, the i.t. injection of DABK or DAKD caused a weak, but prolonged hyperalgesia, an effect that was blocked by the beta(1) receptor antagonist des-Arg(9)-[Leu(8)]-bradykinin (DALBK). the i.t. injection of BK caused thermal hyperalgesia in wild-type mice (WT) and in the beta(1) receptor knockout mice (B1R KO), but not in the beta(2) receptor knockout mice (B2R KO). Similarly, the i.t. injection of DABK elicited thermal hyperalgesia in WT mice, but not in B1R KO mice. However, DABK-induced hyperalgesia was more pronounced in the B,R KO mice when compared with the WT mice. the i.t. injection of Hoe 140 or DALBK inhibited the second phase of formalin (F)-induced nociception. Furthermore, i.t. Hoe 140, but not DALBK, also inhibits the first phase of F response. Finally, the i.t. injection of DALBK, but not of Hoe 140, inhibits the long-term thermal hyperalgesia observed in the ipsilateral and in contralateral paws after intraplantar injection with complete Freund's adjuvant. These findings provide evidence that kinins acting at both B-1 and B-2 receptors at the spinal level exert a critical role in controlling the nociceptive processing mechanisms. Therefore, selective kinin antagonists against both receptors are of potential interest drugs to treat some pain states. (C) 2002 Elsevier B.V. All rights reserved. en
dc.format.extent 1188-1197
dc.language.iso eng
dc.publisher Elsevier B.V.
dc.relation.ispartof Neuropharmacology
dc.rights Acesso restrito
dc.subject kinin en
dc.subject B-1 and B-2 receptor en
dc.subject knockout mice en
dc.subject hyperalgesia en
dc.subject spinal cord en
dc.title The use of kinin B-1 and B-2 receptor knockout mice and selective antagonists to characterize the nociceptive responses caused by kinins at the spinal level en
dc.type Artigo
dc.rights.license http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.contributor.institution Universidade Federal de Santa Catarina (UFSC)
dc.contributor.institution Univ Mogi das Cruzes
dc.contributor.institution MDC Mol Med
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Fed Santa Catarina, Ctr Biol Sci, Dept Pharmacol, Florianopolis, SC, Brazil
dc.description.affiliation Univ Mogi das Cruzes, Mogi Das Cruzes, SP, Brazil
dc.description.affiliation MDC Mol Med, Mol Biol Peptides Hormones Grp, Dept Neurosci, D-13092 Berlin, Germany
dc.description.affiliation Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, SP, Brazil
dc.description.affiliationUnifesp Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, SP, Brazil
dc.identifier.doi 10.1016/S0028-3908(02)00311-8
dc.description.source Web of Science
dc.identifier.wos WOS:000180613400017



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