Deletion of G protein-coupled estrogen receptor increases endothelial vasoconstriction

Hypertension

Volumn 59, Issue 2 SUPPL. 1, 2012, Pages 507-512

  Meyer, Matthias R ^a   Amann, Kerstin ^b   Field, Angela S ^a   Hu, Chelin ^a   Hathaway, Helen J ^a   Kanagy, Nancy L ^a   Walker, Mary K ^c   Barton, Matthias ^d   Prossnitz, Eric R ^a  

^a UNIVERSITY OF NEW MEXICO HEALTH SCIENCES CENTER   (United States)

^b UNIVERSITY OF ERLANGEN NUREMBERG   (Germany)

^c UNIVERSITY OF NEW MEXICO   (United States)

^d UNIVERSITY OF ZURICH   (Switzerland)

Author keywords

cyclooxygenase; EDCF; endothelium; estrogen; GPER; GPR30; prostanoid

Indexed keywords

ENDOTHELIAL NITRIC OXIDE SYNTHASE; G 15; G PROTEIN COUPLED RECEPTOR 30; PROSTANOID; PROSTANOID RECEPTOR; PROTEIN INHIBITOR; THROMBOXANE RECEPTOR; UNCLASSIFIED DRUG; 1,3 BENZODIOXOLE DERIVATIVE; 4 (6 BROMO 1,3 BENZODIOXOL 5 YL) 3A,4,5,9B 3H CYCLOPENTA(C)QUINOLINE; 4-(6-BROMO-1,3-BENZODIOXOL-5-YL)-3A,4,5,9B-3H-CYCLOPENTA(C)QUINOLINE; G PROTEIN COUPLED RECEPTOR; NITRIC OXIDE; QUINOLINE DERIVATIVE; CYCLOOXYGENASE 1; ESTROGEN RECEPTOR; G PROTEIN COUPLED ESTROGEN RECEPTOR; GUANYLATE CYCLASE; PROSTACYCLIN SYNTHASE; SOLUBLE GUANYLATE CYCLASE ALPHA; SOLUBLE GUANYLATE CYCLASE BETA; THROMBOXANE SYNTHASE;

ANIMAL EXPERIMENT; ANIMAL TISSUE; BLOOD VESSEL REACTIVITY; CONFERENCE PAPER; CONTROLLED STUDY; GENE DELETION; GENE EXPRESSION; GENE STRUCTURE; INTRACELLULAR MEMBRANE; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; VASCULAR ENDOTHELIUM; VASOCONSTRICTION; ANIMAL; ARTICLE; DISEASE MODEL; DRUG ANTAGONISM; DRUG EFFECT; GENETICS; METABOLISM; MOUSE MUTANT; PATHOPHYSIOLOGY; PHYSIOLOGY; ANIMAL MODEL; DISEASE ASSOCIATION; ENZYME ACTIVITY; HYPERTENSION; OBESITY; PROTEIN STRUCTURE;

ANIMALS; BENZODIOXOLES; DISEASE MODELS, ANIMAL; ENDOTHELIUM, VASCULAR; GENE DELETION; MALE; MICE; MICE, KNOCKOUT; NITRIC OXIDE; NITRIC OXIDE SYNTHASE TYPE III; QUINOLINES; RECEPTORS, G-PROTEIN-COUPLED; RECEPTORS, THROMBOXANE; VASOCONSTRICTION;

EID: 84856083587     PISSN: 0194911X     EISSN: 15244563     Source Type: Journal    
DOI: 10.1161/HYPERTENSIONAHA.111.184606     Document Type: Conference Paper

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