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

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

Autor Merino, Vanessa F. Autor UNIFESP Google Scholar
Todiras, Mihail Google Scholar
Campos, Luciana A. Google Scholar
Saul, Vera Google Scholar
Popova, Elena Google Scholar
Baltatu, Ovidiu C. Google Scholar
Pesquero, Joao B. Autor UNIFESP Google Scholar
Bader, Michael Google Scholar
Instituição Max Delbruck Ctr Mol Med
Universidade Federal de São Paulo (UNIFESP)
Resumo Two 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.
Assunto transgenic
endothelium
kinin B(1) receptor
endotoxic shock
hypotension
Idioma Inglês
Data 2008-07-01
Publicado em Journal of Molecular Medicine-jmm. New York: Springer, v. 86, n. 7, p. 791-798, 2008.
ISSN 0946-2716 (Sherpa/Romeo, fator de impacto)
Editor Springer
Extensão 791-798
Fonte http://dx.doi.org/10.1007/s00109-008-0345-z
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000257123600007
URI http://repositorio.unifesp.br/handle/11600/30754

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