Evidence that kinin B-2 receptor expression is upregulated by endothelial overexpression of B-1 receptors

Evidence that kinin B-2 receptor expression is upregulated by endothelial overexpression of B-1 receptors

Autor Rodrigues, Eliete da Silva Autor UNIFESP Google Scholar
Silva, Rafael Filippelli da Autor UNIFESP Google Scholar
Martin, Renan Paulo Autor UNIFESP Google Scholar
Oliveira, Suzana Macedo de Autor UNIFESP Google Scholar
Nakaie, Clovis Ryuichi Autor UNIFESP Google Scholar
Sabatini, Regiane Angélica Autor UNIFESP Google Scholar
Merino, Vanessa Ferreira Google Scholar
Pesquero, João Bosco Autor UNIFESP Google Scholar
Bader, Michael Autor UNIFESP Google Scholar
Shimuta, Suma Imura Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Johns Hopkins Univ
Resumo Bradykinin (BK) and des-Arg(9)-bradykinin (DBK) of kallikrein-kinin system exert its effects mediated by the B-2 (B2R) and B-1 (B1R) receptors, respectively. It was already shown that the deletion of kinin B1R or of B2R induces upregulation of the remaining receptor subtype [10,12,16,28,36]. However studies on overexpression of B1R or B2R in transgenic animals have supported the importance of the overexpressed receptor but the expression of another receptor subtype has not been determined [17,19,33]. Previous study described a marked vasodilatation and increased susceptibility to endotoxic shock which was associated with increased mortality in response to DBK in thoracic aorta from transgenic rat overexpressing the kinin B1R (TGR(Tie(2)B(1))) exclusively in the endothelium. in another study, mice overexpressing B1R in multiple tissues were shown to present high susceptibility to inflammation and to lipopolysaccharide-induced endotoxic shock. Therefore the role of B2R was investigated in the thoracic aorta isolated from TGR(Tie(2)B(1)) rats overexpressing the B1R exclusively in the vascular endothelium. Our findings provided evidence for highly increased expression level of the B2R in the transgenic rats. It was reported that under endotoxic shock, these rats exhibited exaggerated hypotension, bradycardia and mortality. It can be suggested that the high mortality during the pathogenesis of endotoxic shock provoked in the transgenic TGR(Tie(2)B(1)) rats could be due to the enhanced expression of B2R associated with the overexpression of the B1R. (c) 2013 Elsevier Inc. All rights reserved.
Palavra-chave AngiotensinII
Bradykinin
des-Arg(9)-bradykinin
Kinin receptors
ACE
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Número do financiamento FAPESP: 2009/08336-2
FAPESP: 2010/05255-9
CNPq: 300247/2010-9
Data de publicação 2013-04-01
Publicado em Peptides. New York: Elsevier B.V., v. 42, p. 1-7, 2013.
ISSN 0196-9781 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 1-7
Fonte http://dx.doi.org/10.1016/j.peptides.2013.01.002
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000320492800001
Endereço permanente http://repositorio.unifesp.br/handle/11600/36109

Exibir registro completo




Arquivo

Nome: WOS000320492800001.pdf
Tamanho: 539.6KB
Formato: PDF
Descrição:
Abrir arquivo

Este item está nas seguintes coleções

Buscar


Navegar

Minha conta