Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/194835
Full metadata record
DC FieldValueLanguage
dc.contributor.CRUESPUNIVERSIDADE DE ESTADUAL DE CAMPINASpt_BR
dc.typeArtigo de periódicopt_BR
dc.titleThe Plasma Protein Extravasation Induced By Adenosine And Its Analogues In The Rat Dorsal Skin: Evidence For The Involvement Of Capsaicin Sensitive Primary Afferent Neurones And Mast Cells.pt_BR
dc.contributor.authorEsquisatto, L Cpt_BR
dc.contributor.authorCosta, S Kpt_BR
dc.contributor.authorCamargo, E Apt_BR
dc.contributor.authorRibela, M Tpt_BR
dc.contributor.authorBrain, S Dpt_BR
dc.contributor.authorde Nucci, Gpt_BR
dc.contributor.authorAntunes, Ept_BR
unicamp.authorL C Esquisatto, Department of Pharmacology, Faculty of Medical Sciences, UNICAMP, PO Box 6111, 13081-970, Campinas, (SP), Brazil.pt_BR
unicamp.author.externalS K Costa,pt
unicamp.author.externalE A Camargo,pt
unicamp.author.externalM T Ribela,pt
unicamp.author.externalS D Brain,pt
unicamp.author.externalG de Nucci,pt
unicamp.author.externalE Antunes,pt
dc.subjectAdenosinept_BR
dc.subjectAdenosine-5'-(n-ethylcarboxamide)pt_BR
dc.subjectAnimalspt_BR
dc.subjectBlood Proteinspt_BR
dc.subjectCapillary Permeabilitypt_BR
dc.subjectCapsaicinpt_BR
dc.subjectDose-response Relationship, Drugpt_BR
dc.subjectFemalept_BR
dc.subjectInjections, Intradermalpt_BR
dc.subjectIsotonic Solutionspt_BR
dc.subjectMalept_BR
dc.subjectMast Cellspt_BR
dc.subjectNeurokinin-1 Receptor Antagonistspt_BR
dc.subjectNeurons, Afferentpt_BR
dc.subjectPeptide Fragmentspt_BR
dc.subjectPiperidinespt_BR
dc.subjectPurinergic P1 Receptor Agonistspt_BR
dc.subjectPurinergic P1 Receptor Antagonistspt_BR
dc.subjectQuinuclidinespt_BR
dc.subjectRatspt_BR
dc.subjectRats, Wistarpt_BR
dc.subjectReceptors, Neurokinin-2pt_BR
dc.subjectSkinpt_BR
dc.subjectSubstance Ppt_BR
dc.subjectTheobrominept_BR
dc.subjectP-methoxy-n-methylphenethylaminept_BR
dc.description.abstract1. The contribution of sensory neurons and mast cells to the oedema evoked by adenosine A1 (N(6)-cyclopentyladenosine, CPA, 3 - 30 nmol site(-1)), A2 (5'N-ethylcarboxamidoadenosine, NECA, 1 - 10 nmol site(-1)) and A3 receptor agonists (N6-[3-iodobenzyl]-N-methyl-5'-carboxiamidoadenosine, IB-MECA, 0.01 - 3 nmol site(-1)) was investigated in the rat skin microvasculature, by the extravascular accumulation of intravenously-injected (i.v.) 125I-albumin. 2. Intradermal (i.d.) injection of adenosine and analogues induced increased microvascular permeability in a dose-dependent manner (IB-MECA > NECA > CPA > adenosine). The non-selective adenosine receptor antagonist theophylline (5 - 50 nmol site(-1)) markedly inhibited adenosine, CPA or NECA but not IB-MECA-induced plasma extravasation. The A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine (DPCPX, 0.3 - 3 micromol kg(-1), i.v.) significantly reduced CPA-induced plasma extravasation whereas responses to adenosine, NECA or IB-MECA were unchanged. The A2 receptor antagonist 3,7-dymethyl-1-proprargylxanthine (DMPX, 0.5 - 50 nmol site(-1)) significantly reduced NECA-induced plasma extravasation without affecting responses to adenosine, CPA and IB-MECA. 3. The 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), but not the NK2 receptor antagonist (S)-N-methyl-N[4-acetylamino-4-phenyl piperidino)-2-(3,4-dichlorophenyl)butyl]-benzamide (SR48968), significantly inhibited the plasma extravasation evoked by higher doses of adenosine (100 nmol site(-1)), CPA (100 nmol site(-1)), NECA (1 nmol site(-1)) and IB-MECA (0.1 - 1 nmol site(-1)). In rats treated with capsaicin to destroy sensory neurons, the response to higher doses of adenosine, CPA and NECA, but not IB-MECA, was significantly inhibited. 4. The effects of adenosine and analogues were largely inhibited by histamine and 5-hydroxytryptamine (5-HT) antagonists and by compound 48/80 pretreatment. 5. In conclusion, our results provide evidence that adenosine A1 and A2, but not A3, receptor agonists may function as cutaneous neurogenic pro-inflammatory mediators; acting via microvascular permeability-increasing mechanisms that can, depending on dose of agonist and purine receptor under study, involve the tachykinin NK1 receptor and mast cell amines.en
dc.relation.ispartofBritish Journal Of Pharmacologypt_BR
dc.relation.ispartofabbreviationBr. J. Pharmacol.pt_BR
dc.date.issued2001-Seppt_BR
dc.identifier.citationBritish Journal Of Pharmacology. v. 134, n. 1, p. 108-15, 2001-Sep.pt_BR
dc.language.isoengpt_BR
dc.description.volume134pt_BR
dc.description.firstpage108-15pt_BR
dc.rightsfechadopt_BR
dc.rights.holderpt_BR
dc.sourcePubMedpt_BR
dc.identifier.issn0007-1188pt_BR
dc.identifier.doi10.1038/sj.bjp.0704245pt_BR
dc.identifier.urlhttp://www.ncbi.nlm.nih.gov/pubmed/11522602pt_BR
dc.date.available2015-11-27T12:28:57Z-
dc.date.accessioned2015-11-27T12:28:57Z-
dc.description.provenanceMade available in DSpace on 2015-11-27T12:28:57Z (GMT). No. of bitstreams: 1 pmed_11522602.pdf: 210109 bytes, checksum: 3c008c849a1d72836eae19948ff5beb4 (MD5) Previous issue date: 2001en
dc.identifier.urihttp://repositorio.unicamp.br/jspui/handle/REPOSIP/194835-
dc.identifier.idPubmed11522602pt_BR
Appears in Collections:Unicamp - Artigos e Outros Documentos

Files in This Item:
File SizeFormat 
pmed_11522602.pdf205.18 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.