Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice

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Item Type:	Article
Title:	Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice
Creators Name:	Xu, P., Costa-Goncalves, A.C., Todiras, M., Rabelo, L.A., Sampaio, W.O., Moura, M.M., Santos, S.S., Luft, F.C., Bader, M., Gross, V., Alenina, N. and Santos, R.A.S.
Abstract:	Mas codes for a G protein-coupled receptor that is implicated in angiotensin-(1-7) signaling. We studied the cardiovascular phenotype of Mas-deficient mice backcrossed onto the FVB/N genetic background using telemetry and found that they exhibit higher blood pressures compared with controls. These Mas(-/-) mice also had impaired endothelial function, decreased NO production, and lower endothelial NO synthase expression. Reduced nicotinamide-adenine dinucleotide phosphate oxidase catalytic subunit gp91(phox) protein content determined by Western blotting was higher in Mas(-/-) mice than in controls, whereas superoxide dismutase and catalase activities were reduced. The superoxide dismutase mimetic, Tempol, decreased blood pressure in Mas(-/-) mice but had a minimal effect in control mice. Our results show a major cardiovascular phenotype in Mas(-/-) mice. Mas-deletion results in increased blood pressure, endothelial dysfunction, and an imbalance between NO and reactive oxygen species. Our animals represent a promising model to study angiotensin-(1-7)-mediated cardiovascular effects and to evaluate Mas agonistic compounds as novel cardioprotective and antihypertensive agents based on their beneficial effects on endothelial function.
Keywords:	Mas-Deficient Mice, Endothelial Function, Ang-(1-7), Reactive Oxygen Species, NO, Animals, Mice
Source:	Hypertension
ISSN:	0194-911X
Publisher:	American Heart Association
Volume:	51
Number:	2
Page Range:	574-580
Date:	February 2008
Official Publication:	https://doi.org/10.1161/HYPERTENSIONAHA.107.102764
PubMed:	View item in PubMed

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