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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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