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Article: Endothelial dysfunction and vascular disease

TitleEndothelial dysfunction and vascular disease
Authors
KeywordsCyclooxygenase
Diabetes
G-proteins
Hypertension
Nitric oxide
Prostanoids
Issue Date2009
PublisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708
Citation
Acta Physiologica, 2009, v. 196 n. 2, p. 193-222 How to Cite?
AbstractThe endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDHF-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive G i (e.g. responses to serotonin and thrombin) and pertussis toxin-insensitive G q (e.g. adenosine diphosphate and bradykinin) coupling proteins. The release of NO by the endothelial cell can be up-regulated (e.g. by oestrogens, exercise and dietary factors) and down-regulated (e.g. oxidative stress, smoking and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively loose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and causing endothelium-dependent hyperpolarizations), endothelial cells also can evoke contraction (constriction) of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factor (EDCF). Most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells. EDCF-mediated responses are exacerbated when the production of NO is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. © 2008 Scandinavian Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/59558
ISSN
2015 Impact Factor: 4.066
2015 SCImago Journal Rankings: 1.690
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorShimokawa, Hen_HK
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorFeletou, Men_HK
dc.date.accessioned2010-05-31T03:52:41Z-
dc.date.available2010-05-31T03:52:41Z-
dc.date.issued2009en_HK
dc.identifier.citationActa Physiologica, 2009, v. 196 n. 2, p. 193-222en_HK
dc.identifier.issn1748-1708en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59558-
dc.description.abstractThe endothelium can evoke relaxations (dilatations) of the underlying vascular smooth muscle, by releasing vasodilator substances. The best characterized endothelium-derived relaxing factor (EDRF) is nitric oxide (NO). The endothelial cells also evoke hyperpolarization of the cell membrane of vascular smooth muscle (endothelium-dependent hyperpolarizations, EDHF-mediated responses). Endothelium-dependent relaxations involve both pertussis toxin-sensitive G i (e.g. responses to serotonin and thrombin) and pertussis toxin-insensitive G q (e.g. adenosine diphosphate and bradykinin) coupling proteins. The release of NO by the endothelial cell can be up-regulated (e.g. by oestrogens, exercise and dietary factors) and down-regulated (e.g. oxidative stress, smoking and oxidized low-density lipoproteins). It is reduced in the course of vascular disease (e.g. diabetes and hypertension). Arteries covered with regenerated endothelium (e.g. following angioplasty) selectively loose the pertussis toxin-sensitive pathway for NO release which favours vasospasm, thrombosis, penetration of macrophages, cellular growth and the inflammatory reaction leading to atherosclerosis. In addition to the release of NO (and causing endothelium-dependent hyperpolarizations), endothelial cells also can evoke contraction (constriction) of the underlying vascular smooth muscle cells by releasing endothelium-derived contracting factor (EDCF). Most endothelium-dependent acute increases in contractile force are due to the formation of vasoconstrictor prostanoids (endoperoxides and prostacyclin) which activate TP receptors of the vascular smooth muscle cells. EDCF-mediated responses are exacerbated when the production of NO is impaired (e.g. by oxidative stress, ageing, spontaneous hypertension and diabetes). They contribute to the blunting of endothelium-dependent vasodilatations in aged subjects and essential hypertensive patients. © 2008 Scandinavian Physiological Society.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708en_HK
dc.relation.ispartofActa Physiologicaen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCyclooxygenaseen_HK
dc.subjectDiabetesen_HK
dc.subjectG-proteinsen_HK
dc.subjectHypertensionen_HK
dc.subjectNitric oxideen_HK
dc.subjectProstanoidsen_HK
dc.subject.meshEndothelium, Vascular - metabolism - physiology - physiopathology-
dc.subject.meshModels, Biological-
dc.subject.meshVascular Diseases - metabolism - physiopathology-
dc.subject.meshVasoconstriction - physiology-
dc.subject.meshVasodilation - physiology-
dc.titleEndothelial dysfunction and vascular diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1748-1708&volume=196&issue=2&spage=193&epage=222&date=2009&atitle=Endothelial+dysfunction+and+vascular+diseaseen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1111/j.1748-1716.2009.01964.xen_HK
dc.identifier.pmid19220204-
dc.identifier.scopuseid_2-s2.0-65449160912en_HK
dc.identifier.hkuros167581en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65449160912&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume196en_HK
dc.identifier.issue2en_HK
dc.identifier.spage193en_HK
dc.identifier.epage222en_HK
dc.identifier.isiWOS:000265613500001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridShimokawa, H=16684837100en_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridFeletou, M=7006461826en_HK
dc.identifier.citeulike4452146-

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