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http://purl.uniprot.org/citations/16415373http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16415373http://www.w3.org/2000/01/rdf-schema#comment"We hypothesized that the downregulation of Cyp2c by tumor necrosis factor (TNF) alpha contributes to hypertension and renal injury in salt-sensitive angiotensin hypertension. Male Sprague-Dawley rats were fed a high-salt diet (8% NaCl), and osmotic minipumps were implanted to deliver angiotensin II for 14 days. Rats were divided into 3 groups: high salt, angiotensin high salt, and angiotensin high salt administered the TNF-alpha blocker, etanercept. Arterial pressure increased from 94+/-5 to 148+/-7 mm Hg during week 1 in the angiotensin high-salt group, whereas etanercept slowed blood pressure elevation during the first week in the treated group (90+/-2 to 109+/-6 mm Hg). After 2 weeks, arterial pressure increased to 156+/-11 mm Hg in the angiotensin high-salt group and 141+/-6 mm Hg in the etanercept-treated group. Albuminuria and proteinuria were significantly elevated in angiotensin high-salt rats and were reduced in the etanercept-treated rats. Urinary monocyte chemoattractant protein-1 excretion significantly increased in the angiotensin high-salt group (275+/-47 versus 81+/-19 ng/day) and was decreased in the etanercept-treated group (153+/-31 ng/day). Angiotensin high-salt rats also had a significant increase in renal monocyte/macrophage infiltration, and this was again attenuated by etanercept treatment. Renal expression of Cyp2c23 decreased, whereas renal epoxide hydrolase expression increased in angiotensin high-salt rats. Etanercept treatment increased Cyp2c23 expression and lowered epoxide hydrolase expression. These data suggest that TNF-alpha contributes to downregulation of Cyp2c23, blood pressure regulation, and renal injury in angiotensin high-salt hypertension."xsd:string
http://purl.uniprot.org/citations/16415373http://purl.org/dc/terms/identifier"doi:10.1161/01.hyp.0000198545.01860.90"xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/author"Imig J.D."xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/author"Pollock D.M."xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/author"Elmarakby A.A."xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/author"Quigley J.E."xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/name"Hypertension"xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/pages"557-562"xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/title"Tumor necrosis factor alpha blockade increases renal Cyp2c23 expression and slows the progression of renal damage in salt-sensitive hypertension."xsd:string
http://purl.uniprot.org/citations/16415373http://purl.uniprot.org/core/volume"47"xsd:string
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http://purl.uniprot.org/citations/16415373http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16415373
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