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Conference Paper: Endothelial dysfunction: From physiology to therapy

TitleEndothelial dysfunction: From physiology to therapy
Authors
Issue Date1999
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmcc
Citation
Journal Of Molecular And Cellular Cardiology, 1999, v. 31 n. 1, p. 61-74 How to Cite?
AbstractThe endothelium controls the tone of the underlying vascular smooth muscle mainly through the production of vasodilator mediators. In some cases, this function is hampered by the release of constrictor substances. The endothelial mediators are also involved in the regulation by the endothelium of vascular architecture and the blood cell-vascular wall interactions. The endothelium-derived factors comprise nitric oxide (NO), prostacyclin, and a still unknown endothelium-derived hyperpolarizing factor(s) (EDHF). In most vascular diseases, the vasodilator function of the endothelium is attenuated. In advanced atherosclerotic lesions, endothelium-dependent vasodilatation may even be abolished. Various degrees and forms of endothelial dysfunction exist, including (1) the impairment of G(αi) proteins, (2) less release of NO, prostacyclin and/or EDHF, (3) increased release of endoperoxides, (4) increased production of reactive oxygen species, (5) increased generation of endothelin-1, and (6) decreased sensitivity of the vascular smooth muscle to NO, prostacyclin and/or EDHF. The levels of bradykinin and angiotensin II within the vascular wall are controlled by angiotensin-conoerting enzyme (ACE). ACE degrades bradykinin and generates angiotensin II. Bradykinin stimulates endothelial cells to release vasodilators. The actions of the kinin are maintained despite endothelial dysfunction, except in very severe arterial lesions. Angiotensin II may be in part responsible for endothelial dysfunction because it induces resistance to the vasodilaor action of NO. Thus, impairment of the generation of angiotensin II blocks the direct and indirect vasoconstrictor effect of the peptide. By potentiating bradykinin, ACE inhibitors promote the release of relaxing vasodilator mediators to restore vasodilator function, and to prevent platelet aggregation as well as the recruitment of leukocytes to the vascular wall.
Persistent Identifierhttp://hdl.handle.net/10722/173536
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.522
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:33Z-
dc.date.available2012-10-30T06:32:33Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Molecular And Cellular Cardiology, 1999, v. 31 n. 1, p. 61-74en_US
dc.identifier.issn0022-2828en_US
dc.identifier.urihttp://hdl.handle.net/10722/173536-
dc.description.abstractThe endothelium controls the tone of the underlying vascular smooth muscle mainly through the production of vasodilator mediators. In some cases, this function is hampered by the release of constrictor substances. The endothelial mediators are also involved in the regulation by the endothelium of vascular architecture and the blood cell-vascular wall interactions. The endothelium-derived factors comprise nitric oxide (NO), prostacyclin, and a still unknown endothelium-derived hyperpolarizing factor(s) (EDHF). In most vascular diseases, the vasodilator function of the endothelium is attenuated. In advanced atherosclerotic lesions, endothelium-dependent vasodilatation may even be abolished. Various degrees and forms of endothelial dysfunction exist, including (1) the impairment of G(αi) proteins, (2) less release of NO, prostacyclin and/or EDHF, (3) increased release of endoperoxides, (4) increased production of reactive oxygen species, (5) increased generation of endothelin-1, and (6) decreased sensitivity of the vascular smooth muscle to NO, prostacyclin and/or EDHF. The levels of bradykinin and angiotensin II within the vascular wall are controlled by angiotensin-conoerting enzyme (ACE). ACE degrades bradykinin and generates angiotensin II. Bradykinin stimulates endothelial cells to release vasodilators. The actions of the kinin are maintained despite endothelial dysfunction, except in very severe arterial lesions. Angiotensin II may be in part responsible for endothelial dysfunction because it induces resistance to the vasodilaor action of NO. Thus, impairment of the generation of angiotensin II blocks the direct and indirect vasoconstrictor effect of the peptide. By potentiating bradykinin, ACE inhibitors promote the release of relaxing vasodilator mediators to restore vasodilator function, and to prevent platelet aggregation as well as the recruitment of leukocytes to the vascular wall.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yjmccen_US
dc.relation.ispartofJournal of Molecular and Cellular Cardiologyen_US
dc.subject.meshAgingen_US
dc.subject.meshAngiotensins - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteriosclerosis - Metabolismen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshEndothelins - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Physiology - Physiopathologyen_US
dc.subject.meshEpoprostenol - Physiologyen_US
dc.subject.meshHeart Failure - Metabolism - Therapyen_US
dc.subject.meshHumansen_US
dc.subject.meshHyperlipidemias - Metabolismen_US
dc.subject.meshHypertension - Metabolism - Therapyen_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMuscle, Smooth, Vascular - Metabolismen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.subject.meshPeptidyl-Dipeptidase A - Physiologyen_US
dc.subject.meshProstaglandins - Physiologyen_US
dc.subject.meshReactive Oxygen Species - Physiologyen_US
dc.subject.meshSignal Transductionen_US
dc.titleEndothelial dysfunction: From physiology to therapyen_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.doi10.1006/jmcc.1998.0844en_US
dc.identifier.pmid10072716-
dc.identifier.scopuseid_2-s2.0-0033055559en_US
dc.identifier.volume31en_US
dc.identifier.issue1en_US
dc.identifier.spage61en_US
dc.identifier.epage74en_US
dc.identifier.isiWOS:000078427700007-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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