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Article: Endothelial dysfunction in diabetes

TitleEndothelial dysfunction in diabetes
Authors
Issue Date2000
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2000, v. 130 n. 5, p. 963-974 How to Cite?
AbstractEndothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of different animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycaemia-induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non-enzymatic glycation and oxidative stress. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to differ according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction.
Persistent Identifierhttp://hdl.handle.net/10722/171236
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDe Vriese, ASen_US
dc.contributor.authorVerbeuren, TJen_US
dc.contributor.authorVan De Voorde, Jen_US
dc.contributor.authorLameire, NHen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:52Z-
dc.date.available2012-10-30T06:12:52Z-
dc.date.issued2000en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2000, v. 130 n. 5, p. 963-974en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171236-
dc.description.abstractEndothelial dysfunction plays a key role in the pathogenesis of diabetic vascular disease. The endothelium controls the tone of the underlying vascular smooth muscle through the production of vasodilator mediators. The endothelium-derived relaxing factors (EDRF) comprise nitric oxide (NO), prostacyclin, and a still elusive endothelium-derived hyperpolarizing factor (EDHF). Impaired endothelium-dependent vasodilation has been demonstrated in various vascular beds of different animal models of diabetes and in humans with type 1 and 2 diabetes. Several mechanisms of endothelial dysfunction have been reported, including impaired signal transduction or substrate availibility, impaired release of EDRF, increased destruction of EDRF, enhanced release of endothelium-derived constricting factors and decreased sensitivity of the vascular smooth muscle to EDRF. The principal mediators of hyperglycaemia-induced endothelial dysfunction may be activation of protein kinase C, increased activity of the polyol pathway, non-enzymatic glycation and oxidative stress. Correction of these pathways, as well as administration of ACE inhibitors and folate, has been shown to improve endothelium-dependent vasodilation in diabetes. Since the mechanisms of endothelial dysfunction appear to differ according to the diabetic model and the vascular bed under study, it is important to select clinically relevant models for future research of endothelial dysfunction.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshDiabetes Mellitus - Physiopathologyen_US
dc.subject.meshEndothelins - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Physiopathologyen_US
dc.subject.meshGlycosylation End Products, Advanced - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshOxidative Stressen_US
dc.subject.meshProtein Kinase C - Physiologyen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshVasodilationen_US
dc.titleEndothelial dysfunction in diabetesen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.bjp.0703393-
dc.identifier.pmid10882379-
dc.identifier.scopuseid_2-s2.0-0033920419en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033920419&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume130en_US
dc.identifier.issue5en_US
dc.identifier.spage963en_US
dc.identifier.epage974en_US
dc.identifier.isiWOS:000088067100002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridDe Vriese, AS=7006417891en_US
dc.identifier.scopusauthoridVerbeuren, TJ=7007006534en_US
dc.identifier.scopusauthoridVan De Voorde, J=7005936690en_US
dc.identifier.scopusauthoridLameire, NH=35375565900en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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