http://purl.uniprot.org/citations/18180400 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/18180400 | http://www.w3.org/2000/01/rdf-schema#comment | "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."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.org/dc/terms/identifier | "doi:10.1161/hypertensionaha.107.102764"xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Xu P."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Bader M."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Alenina N."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Luft F.C."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Todiras M."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Santos R.A."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Gross V."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Santos S.S."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Costa-Goncalves A.C."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Moura M.M."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Rabelo L.A."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/author | "Sampaio W.O."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/name | "Hypertension"xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/pages | "574-580"xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/title | "Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice."xsd:string |
http://purl.uniprot.org/citations/18180400 | http://purl.uniprot.org/core/volume | "51"xsd:string |
http://purl.uniprot.org/citations/18180400 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/18180400 |
http://purl.uniprot.org/citations/18180400 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/18180400 |
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http://purl.uniprot.org/uniprot/#_E0CX40-mappedCitation-18180400 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/18180400 |