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dc.contributor.CRUESPUNIVERSIDADE ESTADUAL DE CAMPINASpt_BR
dc.contributor.authorunicampAntunes, Edsonpt_BR
dc.contributor.authorunicampCosta, Soraia Katia Pereirapt_BR
dc.contributor.authorunicampDe Nucci, Gilbertopt_BR
dc.typeArtigopt_BR
dc.titleInvolvement of vanilloid receptors and purinoceptors in the phoneutria nigriventer spider venom-induced plasma extravasation in rat skinpt_BR
dc.contributor.authorAntunes, E.pt_BR
dc.contributor.authorCosta, S.K.P.pt_BR
dc.contributor.authorBrain, S.D.pt_BR
dc.contributor.authorDe Nucci, G.pt_BR
dc.subjectCanais de cátion TRPVpt_BR
dc.subjectReceptores purinérgicospt_BR
dc.subject.otherlanguageReceptors, Purinergicpt_BR
dc.subject.otherlanguageTRPV cation channelspt_BR
dc.description.abstractPhoneutria nigriventer venom causes stimulation of capsaicin-sensitive primary afferent neurons in the rat dorsal skin, leading to neurogenic plasma protein extravasation due to the release of tachykinin NK1 receptor agonist. In this study we further investigated the mechanisms involved in the venom-induced activation of capsaicin-sensitive primary afferent neurons. The plasma extravasation in response to venom intradermally injected was measured in Wistar rats as the local accumulation of i.v. injected I-125-labelled human serum albumin into skin sites. The tachykinin NK1 receptor agonist, D-Ala-[L-Pro(9),Me-Leu(8)]substance P-(7-11) (GR73632; 10-100 pmol/site), induced a significant plasma leakage that was abolished by the selective tachykinin NK1 receptor antagonist, (S)-1-[2-[3-(3,4-dichlorphenyl)-1 (3-isopropoxyphenylacetyl) piperidin-3-yl] ethyl]-4-phenyl-1 azaniabicyclo [2.2.2]octane chloride (SR140333; 1 nmol/site), whereas the leakage after venom (1-10 mu g/site) was significantly inhibited (but not abolished) by SR140333. The calcitonin gene-related peptide (CGRP) receptor antagonist, CGRP-(8-37), failed to further reduce the residual plasma extravasation induced by venom plus SR140333, The mu-opioid receptor agonist, [D-Ala(2),Me-Phe(4),Gly-ol(5)]enkephalin (DAMGO), and the local anaesthetic, Lignocaine, had no effect on the venom-induced plasma extravasation. Similarly, the L-, N- and P/Q-type voltage-sensitive Ca2+ channel blockers (verapamil, omega-conotoxin MVIIA and MVIIC, respectively) as well as the Na+ channel blockers, tetrodotoxin and carbamazepine, had no effect on the venom-induced effect. Neither the systemic treatment nor the local injection of ruthenium red prevented the venom-induced plasma extravasation. However, the vanilloid receptor antagonist, N-[2-(4-chlorophenyl) ethyl]-1,3,4,5-tetrahydro7,8-dihydroxy-2H-2-benzazepine-2-carbothioamide (capsazepine; 120 mu mol/kg, i.v.), reduced by 48% (P <0.05) the venom (10 mu g/site)-induced plasma extravasation. A significant inhibitory effect was also observed with the P, purinoceptor agonists, adenosine 5'-triphosphate (ATP; 10 and 30 nmol/site) and adenosine 5'-diphosphate (ADP; 10 nmol/site). The involvement of histamine and/or 5-hydroxytryptamine (5-HT) in the venom-induced plasma extravasation was ruled out since neither histamine and 5-HT receptor antagonists nor depletion of mast cells by compound 48/80 affected the venom response. This was further supported by the failure of venom to degranulate in vitro peritoneal mast cells. In conclusion, only vanilloid receptors and P, prejunctional purinoceptors had an inhibitory effect on the neurogenic plasma extravasation evoked by P. nigriventer venom in rat dorsal skinpt
dc.relation.ispartofEuropean journal of pharmacologypt_BR
dc.relation.ispartofabbreviationEur. j. pharmacol.pt_BR
dc.publisher.cityAmsterdam pt_BR
dc.publisher.countryPaíses Baixospt_BR
dc.publisherElsevierpt_BR
dc.date.issued2000pt_BR
dc.date.monthofcirculationMar.pt_BR
dc.identifier.citationEuropean Journal Of Pharmacology. Elsevier Science Bv, v. 391, n. 3, n. 305, n. 315, 2000.pt_BR
dc.language.isoengpt_BR
dc.description.volume391pt_BR
dc.description.issuenumber3pt_BR
dc.description.firstpage305pt_BR
dc.description.lastpage315pt_BR
dc.rightsfechadopt_BR
dc.sourceWeb of Sciencept_BR
dc.identifier.issn0014-2999pt_BR
dc.identifier.eissn1879-0712pt_BR
dc.identifier.doi10.1016/S0014-2999(00)00075-3pt_BR
dc.identifier.urlhttps://www.sciencedirect.com/science/article/pii/S0014299900000753pt_BR
dc.description.sponsorshipFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPpt_BR
dc.description.sponsorship1FAPESP - FUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULOpt_BR
dc.description.sponsordocumentnumbersem informaçãopt_BR
dc.date.available2014-12-02T16:25:03Z
dc.date.available2015-11-26T16:11:54Z-
dc.date.accessioned2014-12-02T16:25:03Z
dc.date.accessioned2015-11-26T16:11:54Z-
dc.description.provenanceMade available in DSpace on 2014-12-02T16:25:03Z (GMT). No. of bitstreams: 1 WOS000086083100015.pdf: 279050 bytes, checksum: 98de72a018ab90415b7a7db55970c8e6 (MD5) Previous issue date: 2000en
dc.description.provenanceMade available in DSpace on 2015-11-26T16:11:54Z (GMT). No. of bitstreams: 2 WOS000086083100015.pdf: 279050 bytes, checksum: 98de72a018ab90415b7a7db55970c8e6 (MD5) WOS000086083100015.pdf.txt: 53488 bytes, checksum: 188e9f7064ede2e0ef86ff9c2c238746 (MD5) Previous issue date: 2000en
dc.identifier.urihttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/60681pt_BR
dc.identifier.urihttp://www.repositorio.unicamp.br/handle/REPOSIP/60681
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/60681-
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.departmentsem informaçãopt_BR
dc.contributor.departmentDepartamento de Farmacologiapt_BR
dc.contributor.unidadeFaculdade de Ciências Médicaspt_BR
dc.identifier.source10729373-
dc.creator.orcid0000-0003-2201-8247pt_BR
dc.creator.orcidsem informaçãopt_BR
dc.creator.orcid0000-0002-4346-7941pt_BR
dc.type.formArtigo originalpt_BR
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