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Article: Chronic mild hyperhomocysteinemia induces aortic endothelial dysfunction but does not elevate arterial pressure in rats

TitleChronic mild hyperhomocysteinemia induces aortic endothelial dysfunction but does not elevate arterial pressure in rats
Authors
KeywordsArterial pressure
Endothelial dysfunction
Homocysteine
Hyperhomocysteinemia
Issue Date2005
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Journal Of Vascular Research, 2005, v. 42 n. 2, p. 148-156 How to Cite?
AbstractMild hyperhomocysteinemia is prevalent in the general population and has been linked to endothelial dysfunction and high arterial pressure (AP) in clinical studies. The present study was designed to determine whether a rise in AP was induced by mild hyperhomocysteinemia and whether the potential rise in AP is secondary or prior to endothelial dysfunction. Experiments were performed in a rat model of mild hyperhomocysteinemia induced by oral administration of homocysteine for 1-4 months. Aortic endothelial dysfunction was observed 2 months after homocysteine treatment while endothelium-independent vasodilation was normal. In parallel, homocysteine treatment increased phenylephrine-induced contraction in aortas with endothelium, but did not modify the contraction in aortas without endothelium, suggesting a decrease of basal NO production. In conscious unrestrained rats, AP was not significantly different 1, 2, 3 and 4 months after homocysteine treatment. In correlation, endothelial function of a resistance vessel (mesenteric artery), mainly non-NO nonprostanoid factor mediated, was preserved, indicating that homocysteine treatment only affected the NO pathway. In conclusion, mild hyperhomocysteinemia alone is not sufficient to elevate arterial blood pressure, at least in the rat model. Aortic endothelial dysfunction produced by mild hyperhomocysteinemia is independent of hemodynamic factors. Copyright © 2005 S. Karger AG.
Persistent Identifierhttp://hdl.handle.net/10722/80277
ISSN
2015 Impact Factor: 2.186
2015 SCImago Journal Rankings: 1.119
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMiao, CYen_HK
dc.contributor.authorVilleneuve, Nen_HK
dc.contributor.authorBrunelJacquemin, Cen_HK
dc.contributor.authorPetit, Cen_HK
dc.contributor.authorGuillaumin, JPen_HK
dc.contributor.authorGransagne, Den_HK
dc.contributor.authorBriant, Cen_HK
dc.contributor.authorVilaine, JPen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:04:31Z-
dc.date.available2010-09-06T08:04:31Z-
dc.date.issued2005en_HK
dc.identifier.citationJournal Of Vascular Research, 2005, v. 42 n. 2, p. 148-156en_HK
dc.identifier.issn1018-1172en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80277-
dc.description.abstractMild hyperhomocysteinemia is prevalent in the general population and has been linked to endothelial dysfunction and high arterial pressure (AP) in clinical studies. The present study was designed to determine whether a rise in AP was induced by mild hyperhomocysteinemia and whether the potential rise in AP is secondary or prior to endothelial dysfunction. Experiments were performed in a rat model of mild hyperhomocysteinemia induced by oral administration of homocysteine for 1-4 months. Aortic endothelial dysfunction was observed 2 months after homocysteine treatment while endothelium-independent vasodilation was normal. In parallel, homocysteine treatment increased phenylephrine-induced contraction in aortas with endothelium, but did not modify the contraction in aortas without endothelium, suggesting a decrease of basal NO production. In conscious unrestrained rats, AP was not significantly different 1, 2, 3 and 4 months after homocysteine treatment. In correlation, endothelial function of a resistance vessel (mesenteric artery), mainly non-NO nonprostanoid factor mediated, was preserved, indicating that homocysteine treatment only affected the NO pathway. In conclusion, mild hyperhomocysteinemia alone is not sufficient to elevate arterial blood pressure, at least in the rat model. Aortic endothelial dysfunction produced by mild hyperhomocysteinemia is independent of hemodynamic factors. Copyright © 2005 S. Karger AG.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVRen_HK
dc.relation.ispartofJournal of Vascular Researchen_HK
dc.rightsJournal of Vascular Research. Copyright © S Karger AG.en_HK
dc.subjectArterial pressureen_HK
dc.subjectEndothelial dysfunctionen_HK
dc.subjectHomocysteineen_HK
dc.subjectHyperhomocysteinemiaen_HK
dc.titleChronic mild hyperhomocysteinemia induces aortic endothelial dysfunction but does not elevate arterial pressure in ratsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1018-1172&volume=42&spage=148&epage=156&date=2005&atitle=Chronic+mild+hyperhomocysteinemia+induces+aortic+endothelial+dysfunction+but+does+not+elevate+arterial+pressure+in+rats+en_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000083972en_HK
dc.identifier.pmid15713986en_HK
dc.identifier.scopuseid_2-s2.0-18044394966en_HK
dc.identifier.hkuros98395en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-18044394966&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume42en_HK
dc.identifier.issue2en_HK
dc.identifier.spage148en_HK
dc.identifier.epage156en_HK
dc.identifier.isiWOS:000228434500007-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridMiao, CY=7103074878en_HK
dc.identifier.scopusauthoridVilleneuve, N=7003458215en_HK
dc.identifier.scopusauthoridBrunelJacquemin, C=8722899200en_HK
dc.identifier.scopusauthoridPetit, C=23103771000en_HK
dc.identifier.scopusauthoridGuillaumin, JP=8722899400en_HK
dc.identifier.scopusauthoridGransagne, D=7801380016en_HK
dc.identifier.scopusauthoridBriant, C=8722899600en_HK
dc.identifier.scopusauthoridVilaine, JP=7004617134en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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