Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/33897
Title: Role of vascular Kinin B-1 and B-2 receptors in endothelial nitric oxide metabolism
Authors: Loiola, Rodrigo Azevedo [UNIFESP]
Reis, Felipe Castellani Gomes dos [UNIFESP]
Mári-Kawamoto, Elisa [UNIFESP]
Scavone, Cristoforo [UNIFESP]
Abdalla, Dulcineia Saes Parra [UNIFESP]
Fernandes, Liliam [UNIFESP]
Pesquero, João Bosco [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Keywords: B-1 receptor
B-2 receptor
Knockout
Bradykinin
Vascular reactivity
Nitric oxide
Issue Date: 1-Aug-2011
Publisher: Elsevier B.V.
Citation: Peptides. New York: Elsevier B.V., v. 32, n. 8, p. 1700-1705, 2011.
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, Ca2+ 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.
URI: http://repositorio.unifesp.br/handle/11600/33897
ISSN: 0196-9781
Other Identifiers: http://dx.doi.org/10.1016/j.peptides.2011.06.010
Appears in Collections:Em verificação - Geral

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