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Article: Enhancement of endothelium dependent relaxation in the rat aortic ring by selenium supplement

TitleEnhancement of endothelium dependent relaxation in the rat aortic ring by selenium supplement
Authors
KeywordsEndothelium dependent relaxation
Rat aortic ring
Selenium supplement
Issue Date1994
PublisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.org
Citation
Cardiovascular Research, 1994, v. 28 n. 3, p. 345-348 How to Cite?
AbstractObjective: The aim was to examine the effect of selenium supplement on endothelium dependent relaxation in rat aortic rings. Methods: Rats were supplemented with selenium for 3 d (intraperitoneal injection of 4.33 μmol sodium selenite · kg -1 body weight · d -1). Saline injections served as controls. Rat aortic ring was precontracted with phenylephrine and endothelium dependent relaxation was produced by the addition of acetylcholine. Results: Acetylcholine-induced endothelium dependent relaxation was enhanced in aortic rings from rats after receiving selenium supplement as compared to control rats. For comparison, endothelium independent vasodilators (sodium nitroprusside and cromakalim) were investigated. Selenium supplement did not affect the relaxation produced by these vasodilators. N-nitro-L-arginine methyl ester (L-NAME) abolished acetylcholine induced relaxation in aortic rings from animals with selenium supplement while indomethacin had no effect on the relaxation. Direct addition of selenium or glutathione peroxidase and glutathione into the organ bath had no effect on acetylcholine induced endothelium dependent relaxation. Conclusions: The enhanced relaxation after selenium supplement was due to an increase in the release of nitric oxide since L-NAME was effective in blocking the relaxation. The lack of an effect by indomethacin indicated little role for cyclooxygenase products in this system. Our results suggest that the effect of selenium supplement on endothelium dependent relaxation is mediated by cellular changes that cannot be mimicked by the direct addition of selenium or the selenium dependent enzyme glutathione peroxidase.
Persistent Identifierhttp://hdl.handle.net/10722/171142
ISSN
2021 Impact Factor: 13.081
2020 SCImago Journal Rankings: 2.774
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLu, Xen_US
dc.contributor.authorLiu, SYen_US
dc.contributor.authorMan, RYKen_US
dc.date.accessioned2012-10-30T06:12:22Z-
dc.date.available2012-10-30T06:12:22Z-
dc.date.issued1994en_US
dc.identifier.citationCardiovascular Research, 1994, v. 28 n. 3, p. 345-348en_US
dc.identifier.issn0008-6363en_US
dc.identifier.urihttp://hdl.handle.net/10722/171142-
dc.description.abstractObjective: The aim was to examine the effect of selenium supplement on endothelium dependent relaxation in rat aortic rings. Methods: Rats were supplemented with selenium for 3 d (intraperitoneal injection of 4.33 μmol sodium selenite · kg -1 body weight · d -1). Saline injections served as controls. Rat aortic ring was precontracted with phenylephrine and endothelium dependent relaxation was produced by the addition of acetylcholine. Results: Acetylcholine-induced endothelium dependent relaxation was enhanced in aortic rings from rats after receiving selenium supplement as compared to control rats. For comparison, endothelium independent vasodilators (sodium nitroprusside and cromakalim) were investigated. Selenium supplement did not affect the relaxation produced by these vasodilators. N-nitro-L-arginine methyl ester (L-NAME) abolished acetylcholine induced relaxation in aortic rings from animals with selenium supplement while indomethacin had no effect on the relaxation. Direct addition of selenium or glutathione peroxidase and glutathione into the organ bath had no effect on acetylcholine induced endothelium dependent relaxation. Conclusions: The enhanced relaxation after selenium supplement was due to an increase in the release of nitric oxide since L-NAME was effective in blocking the relaxation. The lack of an effect by indomethacin indicated little role for cyclooxygenase products in this system. Our results suggest that the effect of selenium supplement on endothelium dependent relaxation is mediated by cellular changes that cannot be mimicked by the direct addition of selenium or the selenium dependent enzyme glutathione peroxidase.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://cardiovascres.oxfordjournals.orgen_US
dc.relation.ispartofCardiovascular Researchen_US
dc.subjectEndothelium dependent relaxation-
dc.subjectRat aortic ring-
dc.subjectSelenium supplement-
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAortaen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshBenzopyrans - Pharmacologyen_US
dc.subject.meshCromakalimen_US
dc.subject.meshCulture Techniquesen_US
dc.subject.meshEndothelium, Vascular - Drug Effectsen_US
dc.subject.meshGlutathione Peroxidase - Pharmacologyen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNg-Nitroarginine Methyl Esteren_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshPyrroles - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSelenium - Pharmacologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleEnhancement of endothelium dependent relaxation in the rat aortic ring by selenium supplementen_US
dc.typeArticleen_US
dc.identifier.emailMan, RYK:rykman@hkucc.hku.hken_US
dc.identifier.authorityMan, RYK=rp00236en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/cvr/28.3.345-
dc.identifier.pmid8174154-
dc.identifier.scopuseid_2-s2.0-0028324990en_US
dc.identifier.volume28en_US
dc.identifier.issue3en_US
dc.identifier.spage345en_US
dc.identifier.epage348en_US
dc.identifier.isiWOS:A1994NA01800008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLu, X=7404839457en_US
dc.identifier.scopusauthoridLiu, SY=24822482600en_US
dc.identifier.scopusauthoridMan, RYK=7004986435en_US
dc.identifier.issnl0008-6363-

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