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Article: Endothelial dysfunction and atherosclerosis

TitleEndothelial dysfunction and atherosclerosis
Authors
Issue Date1997
PublisherOxford University Press. The Journal's web site is located at http://eurheartj.oxfordjournals.org/
Citation
European Heart Journal, 1997, v. 18 SUPPL.5, p. E19-E29 How to Cite?
AbstractThe endothelium mediates a number of responses (relaxation or contraction) of arteries and veins from animals and humans. The endothelium-dependent relaxations are due to the release, by endothelial cells, of potent non-prostanoid vasodilator substances. Among these, the best characterized is endothelium-derived relaxing factor (EDRF), which is believed to be 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 relaxation evoked by EDRF is explained by the stimulation by NO of soluble guanylate cyclase that leads to the accumulation of cGMP. In a number of animal blood vessels and in human coronary arteries, the endothelial cells release a 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 (α2-adrenoceptor activation, serotonin, aggregating platelets, leukotrienes) and insensitive (adenosine diphosphate (ADP), bradykinin) G proteins. In blood vessels from animals with regenerated and reperfused endothelium, and/or atherosclerosis, there is a selective loss of the pertussin toxin-sensitive mechanism of EDRF release, which favours the occurrence of vasospasm, thrombosis and cellular growth. The available information from isolated human blood vessels or obtained in situ concurs with the conclusions reached from studies with isolated animal tissues. In addition to relaxing factors, the endothelial cells can produce contracting factors (endothelium-derived contracting factors; EDCFs) which include superoxide anions, endoperoxides, thromboxane A2 and endothelin. From animal studies it can be concluded that the propensity to release EDCFs is maintained, or even augmented, in diseased blood vessels. The switch from a normally predominant release of EDRFs to that of EDCFs may play a crucial role in atherosclerosis.
Persistent Identifierhttp://hdl.handle.net/10722/171196
ISSN
2015 Impact Factor: 15.064
2015 SCImago Journal Rankings: 6.997
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:38Z-
dc.date.available2012-10-30T06:12:38Z-
dc.date.issued1997en_US
dc.identifier.citationEuropean Heart Journal, 1997, v. 18 SUPPL.5, p. E19-E29en_US
dc.identifier.issn0195-668Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171196-
dc.description.abstractThe endothelium mediates a number of responses (relaxation or contraction) of arteries and veins from animals and humans. The endothelium-dependent relaxations are due to the release, by endothelial cells, of potent non-prostanoid vasodilator substances. Among these, the best characterized is endothelium-derived relaxing factor (EDRF), which is believed to be 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 relaxation evoked by EDRF is explained by the stimulation by NO of soluble guanylate cyclase that leads to the accumulation of cGMP. In a number of animal blood vessels and in human coronary arteries, the endothelial cells release a 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 (α2-adrenoceptor activation, serotonin, aggregating platelets, leukotrienes) and insensitive (adenosine diphosphate (ADP), bradykinin) G proteins. In blood vessels from animals with regenerated and reperfused endothelium, and/or atherosclerosis, there is a selective loss of the pertussin toxin-sensitive mechanism of EDRF release, which favours the occurrence of vasospasm, thrombosis and cellular growth. The available information from isolated human blood vessels or obtained in situ concurs with the conclusions reached from studies with isolated animal tissues. In addition to relaxing factors, the endothelial cells can produce contracting factors (endothelium-derived contracting factors; EDCFs) which include superoxide anions, endoperoxides, thromboxane A2 and endothelin. From animal studies it can be concluded that the propensity to release EDCFs is maintained, or even augmented, in diseased blood vessels. The switch from a normally predominant release of EDRFs to that of EDCFs may play a crucial role in atherosclerosis.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://eurheartj.oxfordjournals.org/en_US
dc.relation.ispartofEuropean Heart Journalen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteriosclerosis - Metabolism - Physiopathologyen_US
dc.subject.meshBiological Factors - Secretionen_US
dc.subject.meshEndothelins - Secretionen_US
dc.subject.meshEndothelium, Vascular - Physiopathology - Secretionen_US
dc.subject.meshGtp-Binding Proteins - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Metabolism - Secretionen_US
dc.titleEndothelial dysfunction and atherosclerosisen_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.doi10.1016/S0195-668X(97)90005-1-
dc.identifier.pmid9402468en_US
dc.identifier.scopuseid_2-s2.0-0030723041en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030723041&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume18en_US
dc.identifier.issueSUPPL.5en_US
dc.identifier.spageE19en_US
dc.identifier.epageE29en_US
dc.identifier.isiWOS:A1997YH07900006-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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