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Conference Paper: Endothelial dysfunction and atherosclerosis | Dysfonctionnement endothelial et atherosclerose

TitleEndothelial dysfunction and atherosclerosis | Dysfonctionnement endothelial et atherosclerose
Authors
Issue Date1997
Citation
Archives Des Maladies Du Coeur Et Des Vaisseaux, 1997, v. 90 SPEC., p. 9-19 How to Cite?
AbstractMammalian endothelium acts as a mediator in arterial and venous relaxation and contraction. Endothelium-dependant relaxation is due to endothelial release of powerful, non-prostanoid vasodilatory substances. The best known of these is the endothelial factor EDRF identified as nitrous oxide (NO). It is the end result of the metabolism of L-arginine by the NO synthetase of endothelial cells. In arterial smooth muscle, the relaxation induced by EDRF is explained by NO stimulation of soluble guanylate cyclase, leading to accumulation of GMPc (cyclic guanosine monophosphate). In some animal vessels and in human coronary arteries, endothelial cells release a substance which induces hyperpolarisation of the cell membrane (endothelial derived hyperpolarising factor, EDHF). Release of EDRF by the cell membrane may be mediated by G proteins sensitive to pertussis toxin (activation of the α2 adrenoreceptor, serotonin, platelet aggregation leukotrienes) or non- sensitive G proteins (adenosine-diphosphate (ADP), bradykinin). In animal blood vessels where the endothelium is regenerated and reperfused, and/or atherosclerotic, a selective loss of the mechanism of EDRF release is observed, sensitive to pertussis toxin, which favorises vasospasm, thrombosis and cellular proliferation. The available data on isolated or in situ human blood vessels concord with studies on isolated animal tissues. In addition to the relaxation factors, endothelial cells can also secreate contracting factors (endothelium derived contracting factors: EDCF): these include superoxide anions, endoparoxides, thromboxane A2 and endothelin. Animal studies indicate that the tendency to release EDCF is maintained or even increased in damaged vessels. The change from normally dominant EDRF release to EDCF release could play an important role in atherosclerosis.
Persistent Identifierhttp://hdl.handle.net/10722/173531
ISSN
2009 Impact Factor: 0.398
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:32Z-
dc.date.available2012-10-30T06:32:32Z-
dc.date.issued1997en_US
dc.identifier.citationArchives Des Maladies Du Coeur Et Des Vaisseaux, 1997, v. 90 SPEC., p. 9-19en_US
dc.identifier.issn0003-9683en_US
dc.identifier.urihttp://hdl.handle.net/10722/173531-
dc.description.abstractMammalian endothelium acts as a mediator in arterial and venous relaxation and contraction. Endothelium-dependant relaxation is due to endothelial release of powerful, non-prostanoid vasodilatory substances. The best known of these is the endothelial factor EDRF identified as nitrous oxide (NO). It is the end result of the metabolism of L-arginine by the NO synthetase of endothelial cells. In arterial smooth muscle, the relaxation induced by EDRF is explained by NO stimulation of soluble guanylate cyclase, leading to accumulation of GMPc (cyclic guanosine monophosphate). In some animal vessels and in human coronary arteries, endothelial cells release a substance which induces hyperpolarisation of the cell membrane (endothelial derived hyperpolarising factor, EDHF). Release of EDRF by the cell membrane may be mediated by G proteins sensitive to pertussis toxin (activation of the α2 adrenoreceptor, serotonin, platelet aggregation leukotrienes) or non- sensitive G proteins (adenosine-diphosphate (ADP), bradykinin). In animal blood vessels where the endothelium is regenerated and reperfused, and/or atherosclerotic, a selective loss of the mechanism of EDRF release is observed, sensitive to pertussis toxin, which favorises vasospasm, thrombosis and cellular proliferation. The available data on isolated or in situ human blood vessels concord with studies on isolated animal tissues. In addition to the relaxation factors, endothelial cells can also secreate contracting factors (endothelium derived contracting factors: EDCF): these include superoxide anions, endoparoxides, thromboxane A2 and endothelin. Animal studies indicate that the tendency to release EDCF is maintained or even increased in damaged vessels. The change from normally dominant EDRF release to EDCF release could play an important role in atherosclerosis.en_US
dc.languageengen_US
dc.relation.ispartofArchives des Maladies du Coeur et des Vaisseauxen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteriosclerosis - Physiopathologyen_US
dc.subject.meshBiological Factors - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Metabolism - Physiopathologyen_US
dc.subject.meshEpoprostenol - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshHypercholesterolemia - Physiopathologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiopathologyen_US
dc.subject.meshNerve Tissue Proteins - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.titleEndothelial dysfunction and atherosclerosis | Dysfonctionnement endothelial et atheroscleroseen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9515109-
dc.identifier.scopuseid_2-s2.0-0031474202en_US
dc.identifier.volume90en_US
dc.identifier.issueSPEC.en_US
dc.identifier.spage9en_US
dc.identifier.epage19en_US
dc.identifier.isiWOS:000071036700002-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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