Endothelial Dysfunction and Elevated Blood Pressure in Mas Gene-Deleted Mice
| العنوان: | Endothelial Dysfunction and Elevated Blood Pressure in Mas Gene-Deleted Mice |
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| المؤلفون: | Mihail Todiras, Sergio Henrique Sousa Santos, Luiza A. Rabelo, Andrey C. da Costa-Goncalves, Michael Bader, Natalia Alenina, Friedrich C. Luft, Robson A.S. Santos, Volkmar Gross, Walkyria O. Sampaio, Marina Matos De Moura, Ping Xu |
| المصدر: | Hypertension. 51:574-580 |
| بيانات النشر: | Ovid Technologies (Wolters Kluwer Health), 2008. |
| سنة النشر: | 2008 |
| مصطلحات موضوعية: | Male, medicine.medical_specialty, Blotting, Western, Biological Availability, Blood Pressure, Mice, Inbred Strains, Nitric Oxide, Proto-Oncogene Mas, Antioxidants, Receptors, G-Protein-Coupled, Cyclic N-Oxides, Superoxide dismutase, Mice, Proto-Oncogene Proteins, Internal medicine, Internal Medicine, medicine, Animals, Endothelial dysfunction, Receptor, Aorta, Mice, Knockout, chemistry.chemical_classification, Oxidase test, Reactive oxygen species, Membrane Glycoproteins, biology, NADPH Oxidases, medicine.disease, Vasodilation, Blot, Oxidative Stress, Phenotype, Endocrinology, chemistry, Catalase, Decreased blood pressure, NADPH Oxidase 2, biology.protein, Spin Labels, Endothelium, Vascular, Reactive Oxygen Species |
| الوصف: | 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. |
| تدمد: | 1524-4563 0194-911X |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::823cd584b034de0c299fa482b4a3f734 https://doi.org/10.1161/hypertensionaha.107.102764 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....823cd584b034de0c299fa482b4a3f734 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15244563 0194911X |
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