Article: Endothelial dysfunction and vascular disease

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TitleEndothelial dysfunction and vascular disease
AuthorsVanhoutte, PM1
Shimokawa, H4
Tang, EHC2
Feletou, M3
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
CitationActa Physiologica, 2009, v. 196 n. 2, p. 193-222 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1748-1716.2009.01964.x
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.
ISSN1748-1708
2011 Impact Factor: 3.09
2011 SCImago Journal Rankings: 0.325
DOIhttp://dx.doi.org/10.1111/j.1748-1716.2009.01964.x
ISI Accession Number IDWOS:000265613500001
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorVanhoutte, PM
dc.contributor.authorShimokawa, H
dc.contributor.authorTang, EHC
dc.contributor.authorFeletou, M
dc.date.accessioned2010-05-31T03:52:41Z
dc.date.available2010-05-31T03:52:41Z
dc.date.issued2009
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.
dc.description.naturepostprint
dc.identifier.citationActa Physiologica, 2009, v. 196 n. 2, p. 193-222 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1748-1716.2009.01964.x
dc.identifier.citeulike4452146
dc.identifier.doihttp://dx.doi.org/10.1111/j.1748-1716.2009.01964.x
dc.identifier.epage222
dc.identifier.hkuros167581
dc.identifier.isiWOS:000265613500001
dc.identifier.issn1748-1708
2011 Impact Factor: 3.09
2011 SCImago Journal Rankings: 0.325
dc.identifier.issue2
dc.identifier.openurl
dc.identifier.pmid19220204
dc.identifier.scopuseid_2-s2.0-65449160912
dc.identifier.spage193
dc.identifier.urihttp://hdl.handle.net/10722/59558
dc.identifier.volume196
dc.languageeng
dc.publisherWiley-Blackwell Publishing Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=1748-1708
dc.publisher.placeUnited Kingdom
dc.relation.ispartofActa Physiologica
dc.relation.referencesReferences in Scopus
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
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.subjectCyclooxygenase
dc.subjectDiabetes
dc.subjectG-proteins
dc.subjectHypertension
dc.subjectNitric oxide
dc.subjectProstanoids
dc.titleEndothelial dysfunction and vascular disease
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. Harvard University
  3. Institut de Recherches Servier, Suresnes
  4. Tohoku University