dc.creatorde Oliveira Fusaro, Maria Cláudia Gonçalves
dc.creatorPelegrini-da-Silva, Adriana
dc.creatorAraldi, Dionéia
dc.creatorParada, Carlos Amílcar
dc.creatorTambeli, Cláudia Herrera
dc.date2010-Dec
dc.date2015-11-27T13:18:14Z
dc.date2015-11-27T13:18:14Z
dc.date.accessioned2018-03-29T01:11:37Z
dc.date.available2018-03-29T01:11:37Z
dc.identifierEuropean Journal Of Pharmacology. v. 649, n. 1-3, p. 177-82, 2010-Dec.
dc.identifier1879-0712
dc.identifier10.1016/j.ejphar.2010.09.037
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/20868656
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/199036
dc.identifier20868656
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1299269
dc.descriptionActivation of peripheral P2X3 and P2X2/3 receptors by endogenous ATP is essential to the development of inflammatory hyperalgesia. We have previously demonstrated that this essential role of P2X3 and P2X2/3 receptors in the development of mechanical hyperalgesia induced by the inflammatory agent carrageenan is mediated by an indirect sensitization of the primary afferent nociceptors dependent on the previous release of tumor necrosis factor alpha (TNF-α) and by a direct sensitization of the primary afferent nociceptors. Therefore, in this study we asked whether activation of P2X3 and P2X2/3 receptors contribute to the mechanical hyperalgesia induced by the inflammatory mediators involved in carrageenan-induced mechanical hyperalgesia, such as bradykinin, tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), chemokine-induced chemoattractant-1 (CINC-1), prostaglandin E₂ (PGE₂) and dopamine. Co-administration of the non-selective P2X3 receptor antagonist TNP-ATP or the selective P2X3 and P2X2/3 receptor antagonist A-317491 with bradykinin, but not with TNF-α, IL-1β, IL-6, CINC-1, PGE₂ or dopamine, prevented in a dose-dependent manner the mechanical hyperalgesia. We also verified whether the activation of P2X3 and P2X2/3 receptors by endogenous ATP contributes to bradykinin-induced mechanical hyperalgesia via neutrophil migration and/or cytokine release. Co-administration of TNP-ATP or A-317491 did not affect either neutrophil migration or the increased concentration of TNF-α, IL-1β, IL-6 and CINC-1 induced by bradykinin. These findings demonstrate that the activation of P2X3 and P2X2/3 receptors by endogenous ATP mediates bradykinin-induced mechanical hyperalgesia by a mechanism that does not depend on neutrophil migration or cytokines release.
dc.description649
dc.description177-82
dc.languageeng
dc.relationEuropean Journal Of Pharmacology
dc.relationEur. J. Pharmacol.
dc.rightsfechado
dc.rightsCopyright © 2010. Published by Elsevier B.V.
dc.sourcePubMed
dc.subjectAdenosine Triphosphate
dc.subjectAnimals
dc.subjectBradykinin
dc.subjectCell Movement
dc.subjectCytokines
dc.subjectDinoprostone
dc.subjectDopamine
dc.subjectHyperalgesia
dc.subjectInflammation
dc.subjectInflammation Mediators
dc.subjectMale
dc.subjectNerve Tissue Proteins
dc.subjectNeurons
dc.subjectNeutrophils
dc.subjectPain Measurement
dc.subjectPurinergic P2x Receptor Antagonists
dc.subjectRats
dc.subjectRats, Wistar
dc.subjectReceptors, Purinergic P2x2
dc.subjectReceptors, Purinergic P2x3
dc.subjectSubcutaneous Tissue
dc.subjectSynaptic Transmission
dc.titleP2x3 And P2x2/3 Receptors Mediate Mechanical Hyperalgesia Induced By Bradykinin, But Not By Pro-inflammatory Cytokines, Pge₂ Or Dopamine.
dc.typeArtículos de revistas


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