| Full text | |
| Author(s): |
Rodrigues, Eliete S.
[1]
;
Silva, Rafael F.
[1]
;
Martin, Renan P.
[1]
;
Oliveira, Suzana M.
[1]
;
Nakaie, Clovis R.
[1]
;
Sabatini, Regiane A.
[2]
;
Merino, Vanessa F.
[3]
;
Pesquero, Joao B.
[1]
;
Bader, Michael
[1]
;
Shimuta, Suma I.
[1]
Total Authors: 10
|
| Affiliation: | [1] Univ Fed Sao Paulo, Dept Biophys, BR-04023062 Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Nephrol, BR-04023062 Sao Paulo - Brazil
[3] Johns Hopkins Univ, Sch Med, Baltimore, MD - USA
Total Affiliations: 3
|
| Document type: | Journal article |
| Source: | Peptides; v. 42, p. 1-7, APR 2013. |
| Web of Science Citations: | 9 |
| 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. (AU) | |
| FAPESP's process: | 09/08336-2 - Role of the extracellular and transmembrane domains to binding and activation of kinin B1 receptor: correlation with the structure-activity of the angiotensin II type I receptor. |
| Grantee: | Eliete da Silva Rodrigues |
| Support Opportunities: | Scholarships in Brazil - Doctorate |
| FAPESP's process: | 10/05255-9 - Role of extracellular and transmembrane domains for binding and activation of kinin B1 receptor and of angiotensin II AT1 receptor: structure-activity correlation |
| Grantee: | Suma Imura Shimuta |
| Support Opportunities: | Regular Research Grants |