Please use this identifier to cite or link to this item: http://repositorio.unifesp.br/handle/11600/36109
Title: Evidence that kinin B-2 receptor expression is upregulated by endothelial overexpression of B-1 receptors
Authors: Rodrigues, Eliete da Silva [UNIFESP]
Silva, Rafael Filippelli da [UNIFESP]
Martin, Renan Paulo [UNIFESP]
Oliveira, Suzana Macedo de [UNIFESP]
Nakaie, Clovis Ryuichi [UNIFESP]
Sabatini, Regiane Angélica [UNIFESP]
Merino, Vanessa Ferreira
Pesquero, João Bosco [UNIFESP]
Bader, Michael [UNIFESP]
Shimuta, Suma Imura [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Johns Hopkins Univ
Keywords: AngiotensinII
Bradykinin
des-Arg(9)-bradykinin
Kinin receptors
ACE
Issue Date: 1-Apr-2013
Publisher: Elsevier B.V.
Citation: Peptides. New York: Elsevier B.V., v. 42, p. 1-7, 2013.
Abstract: 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.
URI: http://repositorio.unifesp.br/handle/11600/36109
ISSN: 0196-9781
Other Identifiers: http://dx.doi.org/10.1016/j.peptides.2013.01.002
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