dc.creatorMARANGONI, RA
dc.creatorANTUNES, E
dc.creatorBRAIN, SD
dc.creatorDENUCCI, G
dc.date1993
dc.dateJUN
dc.date2014-12-16T11:34:28Z
dc.date2015-11-26T17:04:09Z
dc.date2014-12-16T11:34:28Z
dc.date2015-11-26T17:04:09Z
dc.date.accessioned2018-03-28T23:52:23Z
dc.date.available2018-03-28T23:52:23Z
dc.identifierBritish Journal Of Pharmacology. Stockton Press, v. 109, n. 2, n. 539, n. 543, 1993.
dc.identifier0007-1188
dc.identifierWOS:A1993LE28700039
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/54151
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/54151
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/54151
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1279277
dc.description1 The purpose of the present study was to investigate the mechanisms by which venom from Phoneutria nigriventer spider induces increases in vascular permeability in rabbit skin. 2 Local oedema formation, in response to intradermally-injected agents, was measured in male New Zealand white rabbits as the local accumulation of i.v. injected I-125-labelled human serum albumin into skin sites. 3 Phoneutria nigriventer venom (10-30 mug/site) increased vascular permeability, which was inhibited by trasylol (10 mug/site) and the bradykinin B2 receptor antagoniStS D-Arg,[Hyp3,Thi5,8,D-Phe7]-BK (3 nmol/site) and Hoe 140 (0.3 nmol/site). In addition, the oedema induced by the venom was potentiated by the kinase II inhibitor, captopril (1 nmol/site). The lipoxygenase inhibitor, BWA4C (10 nmol/site) and the PAF antagonist, WEB 2086 (100 nmol/site) had no effect on the venom-induced increase in vascular permeability. 4 Incubation of rabbit plasma with Phoneutria nigriventer venom in vitro did not cause bradykinin formation. Further, the plasma kallikrein inhibitor, soybean trypsin inhibitor (10 mug/site), had no effect on the venom-induced increase in vascular permeability in rabbit skin. 5 These results indicate that the oedema produced by Phoneutria nigriventer venom is dependent on the activation of the tissue kallikrein-kinin system.
dc.description109
dc.description2
dc.description539
dc.description543
dc.languageen
dc.publisherStockton Press
dc.publisherBasingstoke
dc.publisherInglaterra
dc.relationBritish Journal Of Pharmacology
dc.relationBr. J. Pharmacol.
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectTRASYLOL
dc.subjectBRADYKININ
dc.subjectKALLIDIN
dc.subjectSOYBEAN TRYPSIN INHIBITOR
dc.subjectCAPTOPRIL
dc.subjectEDEMA
dc.subjectPHONEUTRIA-NIGRIVENTER
dc.subjectIncreased Vascular-permeability
dc.subjectSmooth-muscle
dc.subjectFactor Paf
dc.subjectProstaglandin-e2
dc.subjectInflammation
dc.subjectProstacyclin
dc.subjectAntagonists
dc.subjectInhibition
dc.subjectSynergism
dc.subjectGene
dc.titleACTIVATION BY PHONEUTRIA-NIGRIVENTER (ARMED SPIDER) VENOM OF TISSUE KALLIKREIN-KININOGEN-KININ SYSTEM IN RABBIT SKIN INVIVO
dc.typeArtículos de revistas


Este ítem pertenece a la siguiente institución