| Full text | |
| Author(s): |
Loiola, Rodrigo A.
[1]
;
Reis, Felipe C. G.
[1]
;
Kawamoto, Elisa M.
[2]
;
Scavone, Cristoforo
[2]
;
Abdalla, Dulcineia S.
[3]
;
Fernandes, Liliam
[4]
;
Pesquero, Joao Bosco
[1]
Total Authors: 7
|
| Affiliation: | [1] Univ Fed Sao Paulo, Dept Biophys, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Dept Pharmacol, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo, Dept Clin Anal & Toxicol, Sao Paulo - Brazil
[4] Univ Fed Sao Paulo, Dept Biol Sci, BR-09972270 Diadema, SP - Brazil
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | Peptides; v. 32, n. 8, p. 1700-1705, AUG 2011. |
| Web of Science Citations: | 21 |
| Abstract | |
Kinin B(1) and B(2) receptors play an essential role in inflammatory process and cardiovascular homeostasis. The present study investigated the vascular reactivity and nitric oxide (NO) generation in the isolated mesenteric arteriolar bed from B(1) (B(1)(-/-)) and B(2) receptor (B(2)(-/-)) knockout mice. Endothelial-dependent relaxation was significantly decreased in arterioles from both B(1)(-/-) and B(2)(-/-) in comparison to wild type (WT) mice, with no differences for endothelial-independent relaxating or vasoconstrictor agents. Plasmatic and vascular NO production were markedly reduced in both B(1)(-/-) and B(2)(-/-). In contrast, in the presence of L-arginine, Ca(2+) and co-factors for the enzyme, NO synthase activity was higher in homogenates of mesenteric vessels of B(1)(-/-) and B(2)(-/-). The present study demonstrated that targeted deletion of B(1) or B(2) receptor gene in mice induces important alterations in the vascular reactivity of resistance vessels and NO metabolism. The severe impairment in the endothelial-mediated vasodilation accompanied by decreased NO bioavailability, despite the augmented NOS activity, strongly indicates an exacerbation of NO inactivation in B(1)(-/-) and B(2)(-/-) vessels. The present data provide valuable information in order to clarify the relevance of kinin receptors in regulating vascular physiology and may point to new approaches regarding its correlation with endothelial dysfunction, oxidative stress and NO availability. (C) 2011 Elsevier Inc. All rights reserved. (AU) | |
| FAPESP's process: | 08/06676-8 - Cellular and molecular biology of the kallikrein-kinin and renin-angiotensin systems |
| Grantee: | João Bosco Pesquero |
| Support Opportunities: | Research Projects - Thematic Grants |