| First Author | Xu P | Year | 2008 |
| Journal | Hypertension | Volume | 51 |
| Issue | 2 | Pages | 574-80 |
| PubMed ID | 18180400 | Mgi Jnum | J:283492 |
| Mgi Id | MGI:6382361 | Doi | 10.1161/HYPERTENSIONAHA.107.102764 |
| Citation | Xu P, et al. (2008) Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice. Hypertension 51(2):574-80 |
| abstractText | 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. |
