Increased susceptibility to endotoxic shock in transgenic rats with endothelial overexpression of kinin B(1) receptors

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dc.contributor.authorMerino, Vanessa F. [UNIFESP]
dc.contributor.authorTodiras, Mihail
dc.contributor.authorCampos, Luciana A.
dc.contributor.authorSaul, Vera
dc.contributor.authorPopova, Elena
dc.contributor.authorBaltatu, Ovidiu C.
dc.contributor.authorPesquero, Joao B. [UNIFESP]
dc.contributor.authorBader, Michael
dc.contributor.institutionMax Delbruck Ctr Mol Med
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2016-01-24T13:51:30Z
dc.date.available2016-01-24T13:51:30Z
dc.date.issued2008-07-01
dc.description.abstractTwo kinin receptors have been described, the inducible B(1) and the constitutive B(2). B(1) receptors are important in cardiovascular homeostasis and inflammation. To further clarify their vascular function, we have generated transgenic rats (TGR(Tie2B(1))) overexpressing the B(1) receptor exclusively in the endothelium. Endothelial cell-specific expression was confirmed by B(1)-agonist-induced relaxation of isolated aorta, which was abolished by endothelial denudation of the vessel. This vasodilatation was mediated by nitric oxide (NO) and K(+) channels. TGR(Tie2B(1)) rats were normotensive but, in contrast to controls, reacted with a marked fall in blood pressure and increased vascular permeability after intravenous injection of a B(1) agonist. After lipopolysaccharide treatment, they present a more pronounced hypotensive response and marked bradycardia associated with increased mortality when compared to non-transgenic control animals. Thus, the transgenic rats overexpressing kinin B(1) receptors exclusively in the endothelium generated in this study support an important role of this receptor in the vasculature during the pathogenesis of endotoxic shock.en
dc.description.affiliationMax Delbruck Ctr Mol Med, D-13125 Berlin, Germany
dc.description.affiliationUniversidade Federal de São Paulo, São Paulo, Brazil
dc.description.affiliationUnifespUniversidade Federal de São Paulo, São Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent791-798
dc.identifierhttp://dx.doi.org/10.1007/s00109-008-0345-z
dc.identifier.citationJournal of Molecular Medicine-jmm. New York: Springer, v. 86, n. 7, p. 791-798, 2008.
dc.identifier.doi10.1007/s00109-008-0345-z
dc.identifier.issn0946-2716
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/30754
dc.identifier.wosWOS:000257123600007
dc.language.isoeng
dc.publisherSpringer
dc.relation.ispartofJournal of Molecular Medicine-jmm
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.rights.licensehttp://www.springer.com/open+access/authors+rights?SGWID=0-176704-12-683201-0
dc.subjecttransgenicen
dc.subjectendotheliumen
dc.subjectkinin B(1) receptoren
dc.subjectendotoxic shocken
dc.subjecthypotensionen
dc.titleIncreased susceptibility to endotoxic shock in transgenic rats with endothelial overexpression of kinin B(1) receptorsen
dc.typeinfo:eu-repo/semantics/article
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