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Article: Endothelial dysfunction and vascular disease.

TitleEndothelial dysfunction and vascular disease.
Authors
Issue Date1998
Citation
Verhandelingen - Koninklijke Academie Voor Geneeskunde Van België, 1998, v. 60 n. 3, p. 251-266 How to Cite?
AbstractThe endothelium plays an obligatory role in a number of relaxations of isolated arteries. These endothelium-dependent relaxations are due to the release by the endothelial cells of potent vasodilator substances [endothelium-derived relaxing factors (EDRF)]. The best characterized EDRF is nitric oxide (NO). Nitric oxide is formed by the metabolism of L-arginine by the constitutive NO synthase of endothelial cells. In arterial smooth muscle, the relaxations evoked by EDRF are explained best by the stimulation by NO of soluble guanylate cyclase that leads to the accumulation of cyclic GMP. The endothelial cells also release an unidentified substance that causes hyperpolarization of the cell membrane (endothelium-derived hyperpolarizing factor, EDHF). The release of EDRF from the endothelium can be mediated by both pertussis toxin-sensitive (alpha2-adrenergic activation, serotonin, thrombin, aggregating platelets) and insensitive (adenosine diphosphate, bradykinin) G-proteins. In blood vessels from animals with regenerated endothelium, and/or atherosclerosis, there is a selective loss of the pertussis-toxin sensitive mechanism of EDRF-release which favors the occurrence of vasospasm, thrombosis and cellular growth.
Persistent Identifierhttp://hdl.handle.net/10722/171207
ISSN
2014 SCImago Journal Rankings: 0.135

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:42Z-
dc.date.available2012-10-30T06:12:42Z-
dc.date.issued1998en_US
dc.identifier.citationVerhandelingen - Koninklijke Academie Voor Geneeskunde Van België, 1998, v. 60 n. 3, p. 251-266en_US
dc.identifier.issn0302-6469en_US
dc.identifier.urihttp://hdl.handle.net/10722/171207-
dc.description.abstractThe endothelium plays an obligatory role in a number of relaxations of isolated arteries. These endothelium-dependent relaxations are due to the release by the endothelial cells of potent vasodilator substances [endothelium-derived relaxing factors (EDRF)]. The best characterized EDRF is nitric oxide (NO). Nitric oxide is formed by the metabolism of L-arginine by the constitutive NO synthase of endothelial cells. In arterial smooth muscle, the relaxations evoked by EDRF are explained best by the stimulation by NO of soluble guanylate cyclase that leads to the accumulation of cyclic GMP. The endothelial cells also release an unidentified substance that causes hyperpolarization of the cell membrane (endothelium-derived hyperpolarizing factor, EDHF). The release of EDRF from the endothelium can be mediated by both pertussis toxin-sensitive (alpha2-adrenergic activation, serotonin, thrombin, aggregating platelets) and insensitive (adenosine diphosphate, bradykinin) G-proteins. In blood vessels from animals with regenerated endothelium, and/or atherosclerosis, there is a selective loss of the pertussis-toxin sensitive mechanism of EDRF-release which favors the occurrence of vasospasm, thrombosis and cellular growth.en_US
dc.languageengen_US
dc.relation.ispartofVerhandelingen - Koninklijke Academie voor Geneeskunde van Belgiëen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Vessels - Physiology - Physiopathologyen_US
dc.subject.meshEndothelium, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshHumansen_US
dc.subject.meshModels, Cardiovascularen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshVascular Diseases - Physiopathologyen_US
dc.titleEndothelial dysfunction and vascular disease.en_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.pmid9803882-
dc.identifier.scopuseid_2-s2.0-0031615089en_US
dc.identifier.volume60en_US
dc.identifier.issue3en_US
dc.identifier.spage251en_US
dc.identifier.epage266en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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