Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/193724
Type: Artigo de periódico
Title: Activation Of Tissue Kallikrein-kininogen-kinin System In Rabbit Skin By A Fraction Isolated From Phoneutria Nigriventer (armed Spider) Venom.
Author: Antunes, E
Marangoni, R A
Giglio, J R
Brain, S D
de Nucci, G
Abstract: Phoneutria nigriventer venom was fractionated by gel filtration followed by ion-exchange chromatography from which 16 fractions (I-XVI) were obtained and assayed in rabbit skin in order to identify those responsible for the increased vascular permeability observed with the whole venom. The fractions, and control mediators (tissue kallikrein, bradykinin and histamine) were intradermally injected in male New Zealand white rabbits. Local oedema formation was measured as the local accumulation of i.v. injected 125I-human serum albumin into skin sites. Fraction XIII was the only fraction assayed which significantly induced oedema formation. Fraction XIII-induced oedema was greatly reduced by either the protease inhibitor aprotinin or the bradykinin B2 receptor antagonist D-Arg,[Hyp3,Thi5,8D-Phe7]-Bk, whereas the plasma kallikrein inhibitor soybean trypsin inhibitor failed to significantly affect this oedematogenic response. The kininase II inhibitor captopril markedly potentiated fraction XIII-induced oedema. Our results indicate that the increased vascular permeability induced by fraction XIII is due to local generation of kinins in response to tissue (but not plasma) kallikrein-kinin system activation.
Subject: Animals
Capillary Permeability
Edema
Kallikrein-kinin System
Male
Rabbits
Skin
Spider Venoms
Rights: fechado
Identifier DOI: 
Address: http://www.ncbi.nlm.nih.gov/pubmed/8310440
Date Issue: 1993
Appears in Collections:Artigos e Materiais de Revistas Científicas - Unicamp

Files in This Item:
File SizeFormat 
pmed_8310440.pdf442.61 kBAdobe PDFView/Open


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