| http://purl.uniprot.org/citations/16183707 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/16183707 | http://www.w3.org/2000/01/rdf-schema#comment | "The present study was designed to analyze the effect of long-term incubation with interleukin-1beta (IL-1beta) on endothelium-dependent relaxation in rat mesenteric resistance arteries. Vessels were incubated in culture medium with or without IL-1beta (10 ng/ml, 14 h). Changes in lumen diameter were recorded in a pressure myograph. Protein expression, nitrite, and superoxide anion (O(2)(.)) production were evaluated by either Western blot or immunofluorescence, Griess reaction, and ethidium fluorescence, respectively. IL-1beta impaired acetylcholine (ACh) and sodium nitroprusside (SNP) vasodilation and increased nitrite and O(2)(.) production and inducible nitric-oxide synthase (iNOS), xanthine oxidase, and p22(phox) expression. However, neither endothelial nitric-oxide synthase (NOS) nor soluble guanylate cyclase protein expression were affected by IL-1beta treatment. Polyethylene glycol superoxide dismutase partially reversed the impairment of ACh relaxation and abolished the O(2)(.) production observed in IL-1beta-treated arteries. The impairment of ACh relaxation induced by IL-1beta was also partially reversed by the xanthine oxidase inhibitor allopurinol (1 mM) but not by either the NADPH oxidase inhibitor apocynin (0.3 mM) or the inducible NOS inhibitor N-3-aminomethylbenzylacetamidine (1 microM). However, all these inhibitors improved the impaired SNP response. The results of the present study demonstrate that long-term incubation with IL-1beta induces an impairment of the nitric oxide-mediated relaxation in mesenteric resistance arteries through the production of O(2)(.), mainly from xanthine oxidase."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.org/dc/terms/identifier | "doi:10.1124/jpet.105.088435"xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/author | "Giraldo J."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/author | "Planas A.M."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/author | "Briones A.M."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/author | "Vila E."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/author | "Salaices M."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/author | "Jimenez-Altayo F."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/date | "2006"xsd:gYear |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/name | "J Pharmacol Exp Ther"xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/pages | "42-52"xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/title | "Increased superoxide anion production by interleukin-1beta impairs nitric oxide-mediated relaxation in resistance arteries."xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://purl.uniprot.org/core/volume | "316"xsd:string |
| http://purl.uniprot.org/citations/16183707 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/16183707 |
| http://purl.uniprot.org/citations/16183707 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/16183707 |
| http://purl.uniprot.org/uniprot/Q62737#attribution-439354E13F61C9C415FB7C2A02C1DD99 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/16183707 |
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| http://purl.uniprot.org/uniprot/Q62737 | http://purl.uniprot.org/core/mappedCitation | http://purl.uniprot.org/citations/16183707 |
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