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Article: Endothelial dysfunction and vascular pathology | Dysfonctionnement endothélial et pathologie vasculaire.

TitleEndothelial dysfunction and vascular pathology | Dysfonctionnement endothélial et pathologie vasculaire.
Authors
Issue Date2006
PublisherAcademie Royale de Medecine de Belgique.
Citation
Bulletin Et Mémoires De L'académie Royale De Médecine De Belgique, 2006, v. 161 n. 10-12, p. 529-536; discussion 536-537 How to Cite?
AbstractEndothelium-dependent relaxations are due to the release by the endothelial cells of potent vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO), from 1-arginine by the constitutive endothelial NO synthase. In arterial smooth muscle, NO stimulates soluble guanylate cyclase which leads to the accumulation of cyclic GMP. Endothelial cells also release substances (EDHF) that hyperpolarize vascular smooth muscle. The release of NO from the endothelium can be mediated by both Gi (catecholamines, serotonin, thrombin) and Gq (adenosine diphosphate, bradykinin) G-proteins. In arteries with regenerated endothelium and/or atherosclerosis, there is a selective loss of the Gi mechanism of No-release which favours the occurrence of vasospasm, thrombosis and cellular growth. In addition to relaxing factors, the endothelial cells can produce contracting-substances (EDCF) which include superoxide anions, endoperoxides, thromboxane A2 and endothelin-1. The propensity to release EDCFs is maintained or even augmented in diseased blood vessels. The switch from a normally predominant release of NO to that of EDCF may play a crucial role in vascular disease.
Persistent Identifierhttp://hdl.handle.net/10722/80253
ISSN
2014 SCImago Journal Rankings: 0.104

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:04:14Z-
dc.date.available2010-09-06T08:04:14Z-
dc.date.issued2006en_HK
dc.identifier.citationBulletin Et Mémoires De L'académie Royale De Médecine De Belgique, 2006, v. 161 n. 10-12, p. 529-536; discussion 536-537en_HK
dc.identifier.issn0377-8231en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80253-
dc.description.abstractEndothelium-dependent relaxations are due to the release by the endothelial cells of potent vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO), from 1-arginine by the constitutive endothelial NO synthase. In arterial smooth muscle, NO stimulates soluble guanylate cyclase which leads to the accumulation of cyclic GMP. Endothelial cells also release substances (EDHF) that hyperpolarize vascular smooth muscle. The release of NO from the endothelium can be mediated by both Gi (catecholamines, serotonin, thrombin) and Gq (adenosine diphosphate, bradykinin) G-proteins. In arteries with regenerated endothelium and/or atherosclerosis, there is a selective loss of the Gi mechanism of No-release which favours the occurrence of vasospasm, thrombosis and cellular growth. In addition to relaxing factors, the endothelial cells can produce contracting-substances (EDCF) which include superoxide anions, endoperoxides, thromboxane A2 and endothelin-1. The propensity to release EDCFs is maintained or even augmented in diseased blood vessels. The switch from a normally predominant release of NO to that of EDCF may play a crucial role in vascular disease.en_HK
dc.languageengen_HK
dc.publisherAcademie Royale de Medecine de Belgique.en_HK
dc.relation.ispartofBulletin et mémoires de l'Académie royale de médecine de Belgiqueen_HK
dc.titleEndothelial dysfunction and vascular pathology | Dysfonctionnement endothélial et pathologie vasculaire.en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0377-8231&volume=161&spage=529&epage=537&date=2006&atitle=Dysfonctionnement+Endothelial+Et+Pathologie+Vasculaireen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid17503729-
dc.identifier.scopuseid_2-s2.0-34249948613en_HK
dc.identifier.hkuros136349en_HK
dc.identifier.volume161en_HK
dc.identifier.issue10-12en_HK
dc.identifier.spage529en_HK
dc.identifier.epage536; discussion 536en_HK
dc.publisher.placeBelgiumen_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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