Endothelial dysfunction and elevated blood pressure in Mas gene-deleted mice

Hypertension

Volumn 51, Issue 2 PART 2, 2008, Pages 574-580

  Xu, Ping ^a   Costa Goncalves, Andrey C ^a,b   Todiras, Mihail ^a   Rabelo, Luiza A ^b,c   Sampaio, Walkyria O ^b   Moura, Marina M ^b   Santos, Sergio Sousa ^b   Luft, Friedrich C ^a,d   Bader, Michael ^a   Gross, Volkmar ^a   Alenina, Natalia ^a   Santos, Robson A S ^b  

^a MAX DELBRÜCK CENTER FOR MOLECULAR MEDICINE   (Germany)

^b FEDERAL UNIVERSITY OF MINAS GERAIS   (Brazil)

^c FEDERAL UNIVERSITY OF ALAGOAS   (Brazil)

^d CHARITÉ UNIVERSITÄTSMEDIZIN BERLIN   (Germany)

Author keywords

Ang (1 7); Endothelial function; Mas deficient mice; NO; Reactive oxygen species

Indexed keywords

ANGIOTENSIN[1-7]; CATALASE; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; REACTIVE OXYGEN METABOLITE; REDUCED NICOTINAMIDE ADENINE DINUCLEOTIDE PHOSPHATE OXIDASE 2; SUPEROXIDE DISMUTASE; TEMPOL;

ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; CARDIOVASCULAR FUNCTION; CONFERENCE PAPER; CONTROLLED STUDY; ENDOTHELIAL DYSFUNCTION; GENE DELETION; HYPERTENSION; MALE; MOUSE; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; TELEMETRY; WESTERN BLOTTING;

ANIMALS; ANTIOXIDANTS; AORTA; BIOLOGICAL AVAILABILITY; BLOOD PRESSURE; BLOTTING, WESTERN; CYCLIC N-OXIDES; ENDOTHELIUM, VASCULAR; MALE; MEMBRANE GLYCOPROTEINS; MICE; MICE, INBRED STRAINS; MICE, KNOCKOUT; NADPH OXIDASE; NITRIC OXIDE; OXIDATIVE STRESS; PHENOTYPE; PROTO-ONCOGENE PROTEINS; REACTIVE OXYGEN SPECIES; RECEPTORS, G-PROTEIN-COUPLED; SPIN LABELS; VASODILATION;

EID: 38549174602     PISSN: 0194911X     EISSN: None     Source Type: Journal    
DOI: 10.1161/HYPERTENSIONAHA.107.102764     Document Type: Conference Paper

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