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|Type:||Artigo de periódico|
|Title:||Increased Vascular Contractility And Oxidative Stress In β 2-adrenoceptor Knockout Mice: The Role Of Nadph Oxidase|
|Abstract:||Background/Aims: β 2-adrenoceptor (β 2-AR) activation induces smooth muscle relaxation and endothelium-derived nitric oxide (NO) release. However, whether endogenous basal β 2-AR activity controls vascular redox status and NO bioavailability is unclear. Thus, we aimed to evaluate vascular reactivity in mice lacking functional β 2- AR (β 2KO), focusing on the role of NO and superoxide anion. Methods and Results: Isolated thoracic aortas from β 2KO and wild-type mice (WT) were studied. β 2KO aortas exhibited an enhanced contractile response to phenylephrine compared to WT. Endothelial removal and L-NAME incubation increased phenylephrine-induced contraction, abolishing the differences between β 2KO and WT mice. Basal NO availability was reduced in aortas from β 2KO mice. Incubation of β 2KO aortas with superoxide dismutase or NADPH inhibitor apocynin restored the enhanced contractile response to phenylephrine to WT levels. β 2KO aortas exhibited oxidative stress detected by enhanced dihydroethidium fluorescence, which was normalized by apocynin. Protein expression of eNOS was reduced, while p47 phox expression was enhanced in β 2KO aortas. Conclusions: The present results demonstrate for the first time that enhanced NADPH-derived superoxide anion production is associated with reduced NO bioavailability in aortas of β 2KO mice. This study extends the knowledge of the relevance of the endogenous activity of β 2-AR to the maintenance of the vascular physiology. © 2012 S. Karger AG, Basel.|
|Appears in Collections:||Unicamp - Artigos e Outros Documentos|
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