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Article: Endothelial dysfunction - The first step toward coronary arteriosclerosis

TitleEndothelial dysfunction - The first step toward coronary arteriosclerosis
Authors
KeywordsArteriosclerosis
Endothelium
Endothelium-derived relaxing factors
Vasodilatation
Issue Date2009
PublisherJapanese Circulation Society. The Journal's web site is located at http://www.j-circ.or.jp/english/publications/
Citation
Circulation Journal, 2009, v. 73 n. 4, p. 595-601 How to Cite?
AbstractThe endothelium causes relaxations of the underlying vascular smooth muscle, by releasing nitric oxide (NO). The endothelial cells also can evoke hyperpolarization of the vascular smooth muscle cells (endothelium-dependent hyperpolarizations, endothelium-derived hyperpolarizing factors-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive Gi and pertussis toxin-insensitive Gq coupling proteins. The endothelial release of NO is reduced in diabetes and hypertension. Arteries covered with regenerated endothelium lose the pertussis-toxin sensitive pathway for NO-release. This dysfunction favors vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. Endothelial cells also release endothelium-derived contracting factors (EDCF). Most endothelium-dependent contractions are mediated by vasoconstrictor prostanoids (endoperoxides and prostacyclin), which activate thromboxane-prostanoid (TP)-receptors of the underlying vascular smooth muscle cells. EDCF-mediated responses are augmented by aging, hypertension and diabetes. Thus, endothelial dysfunction is the first step toward coronary arteriosclerosis.
Persistent Identifierhttp://hdl.handle.net/10722/59542
ISSN
2015 Impact Factor: 4.124
2015 SCImago Journal Rankings: 1.728
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-05-31T03:52:23Z-
dc.date.available2010-05-31T03:52:23Z-
dc.date.issued2009en_HK
dc.identifier.citationCirculation Journal, 2009, v. 73 n. 4, p. 595-601en_HK
dc.identifier.issn1346-9843en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59542-
dc.description.abstractThe endothelium causes relaxations of the underlying vascular smooth muscle, by releasing nitric oxide (NO). The endothelial cells also can evoke hyperpolarization of the vascular smooth muscle cells (endothelium-dependent hyperpolarizations, endothelium-derived hyperpolarizing factors-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive Gi and pertussis toxin-insensitive Gq coupling proteins. The endothelial release of NO is reduced in diabetes and hypertension. Arteries covered with regenerated endothelium lose the pertussis-toxin sensitive pathway for NO-release. This dysfunction favors vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. Endothelial cells also release endothelium-derived contracting factors (EDCF). Most endothelium-dependent contractions are mediated by vasoconstrictor prostanoids (endoperoxides and prostacyclin), which activate thromboxane-prostanoid (TP)-receptors of the underlying vascular smooth muscle cells. EDCF-mediated responses are augmented by aging, hypertension and diabetes. Thus, endothelial dysfunction is the first step toward coronary arteriosclerosis.en_HK
dc.languageengen_HK
dc.publisherJapanese Circulation Society. The Journal's web site is located at http://www.j-circ.or.jp/english/publications/en_HK
dc.relation.ispartofCirculation Journalen_HK
dc.subjectArteriosclerosisen_HK
dc.subjectEndotheliumen_HK
dc.subjectEndothelium-derived relaxing factorsen_HK
dc.subjectVasodilatationen_HK
dc.titleEndothelial dysfunction - The first step toward coronary arteriosclerosisen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1346-9843&volume=2009, 73&issue=4&spage=595&epage=601&date=2009&atitle=Endothelial+Dysfunction+-+The+first+step+toward+coronary+arteriosclerosisen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1253/circj.CJ-08-1169en_HK
dc.identifier.pmid19225203-
dc.identifier.scopuseid_2-s2.0-65649110801en_HK
dc.identifier.hkuros166657en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65649110801&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume73en_HK
dc.identifier.issue4en_HK
dc.identifier.spage595en_HK
dc.identifier.epage601en_HK
dc.identifier.isiWOS:000264733000001-
dc.publisher.placeJapanen_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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