RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/18180400http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/18180400http://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/18180400http://purl.org/dc/terms/identifier"doi:10.1161/hypertensionaha.107.102764"xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Xu P."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Bader M."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Alenina N."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Luft F.C."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Todiras M."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Santos R.A."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Gross V."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Santos S.S."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Costa-Goncalves A.C."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Moura M.M."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Rabelo L.A."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/author"Sampaio W.O."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/date"2008"xsd:gYear
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/name"Hypertension"xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/pages"574-580"xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/title"Endothelial dysfunction and elevated blood pressure in MAS gene-deleted mice."xsd:string
http://purl.uniprot.org/citations/18180400http://purl.uniprot.org/core/volume"51"xsd:string
http://purl.uniprot.org/citations/18180400http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/18180400
http://purl.uniprot.org/citations/18180400http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/18180400
http://purl.uniprot.org/uniprot/#_E0CYD1-mappedCitation-18180400http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18180400
http://purl.uniprot.org/uniprot/#_Q0VB49-mappedCitation-18180400http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18180400
http://purl.uniprot.org/uniprot/#_E0CX40-mappedCitation-18180400http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/18180400