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Article: The endothelium in health and disease

TitleThe endothelium in health and disease
Authors
Issue Date1994
Citation
Texas Heart Institute Journal, 1994, v. 21 n. 1, p. 62-67 How to Cite?
AbstractThe early observations of an apparent anomalous action of acetylcholine on the regulation of vascular tone in vivo and in vitro were found to be a reflection of the intactness of the endothelium in vivo. An intact endothelium mediates relaxation of smooth muscle in response to acetylcholine, whereas endothelium-denuded blood vessels exposed to this agonist often exhibit vasoconstriction. The vasodilation is mediated by the actions of the endothelium-derived relaxing factors nitric oxide and prostacyclin. In addition, endothelial cells release endothelium-derived hyperpolarizing factor, which regulates potassium-channel opening in vascular smooth muscle. The chemical nature of this molecule remains to be elucidated. Many of the physiologic stimulants for endothelium-derived relaxing factor production are released by aggregating platelets, and the significance of the endothelium's vasoprotective role becomes apparent when the mechanisms and consequences of platelet agglutination are studied. Damage to the endothelium, however minor, results in the loss of this protective function and is associated with an impaired response to serotonin of G-protein coupled receptors. In the presence of risk factors such as elevated serum cholesterol, the consequences of an impaired endothelial function are greatly enhanced. Age-related changes in endothelial responsiveness may account for the prevalence of cardiovascular disease in human beings over the age of 30 years.
Persistent Identifierhttp://hdl.handle.net/10722/171141
ISSN
2023 Impact Factor: 0.8
2023 SCImago Journal Rankings: 0.250
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorScottBurden, Ten_US
dc.date.accessioned2012-10-30T06:12:22Z-
dc.date.available2012-10-30T06:12:22Z-
dc.date.issued1994en_US
dc.identifier.citationTexas Heart Institute Journal, 1994, v. 21 n. 1, p. 62-67en_US
dc.identifier.issn0730-2347en_US
dc.identifier.urihttp://hdl.handle.net/10722/171141-
dc.description.abstractThe early observations of an apparent anomalous action of acetylcholine on the regulation of vascular tone in vivo and in vitro were found to be a reflection of the intactness of the endothelium in vivo. An intact endothelium mediates relaxation of smooth muscle in response to acetylcholine, whereas endothelium-denuded blood vessels exposed to this agonist often exhibit vasoconstriction. The vasodilation is mediated by the actions of the endothelium-derived relaxing factors nitric oxide and prostacyclin. In addition, endothelial cells release endothelium-derived hyperpolarizing factor, which regulates potassium-channel opening in vascular smooth muscle. The chemical nature of this molecule remains to be elucidated. Many of the physiologic stimulants for endothelium-derived relaxing factor production are released by aggregating platelets, and the significance of the endothelium's vasoprotective role becomes apparent when the mechanisms and consequences of platelet agglutination are studied. Damage to the endothelium, however minor, results in the loss of this protective function and is associated with an impaired response to serotonin of G-protein coupled receptors. In the presence of risk factors such as elevated serum cholesterol, the consequences of an impaired endothelial function are greatly enhanced. Age-related changes in endothelial responsiveness may account for the prevalence of cardiovascular disease in human beings over the age of 30 years.en_US
dc.languageengen_US
dc.relation.ispartofTexas Heart Institute Journalen_US
dc.subject.meshBlood Platelets - Physiologyen_US
dc.subject.meshEndothelins - Physiologyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshEpoprostenol - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Physiologyen_US
dc.titleThe endothelium in health and diseaseen_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.pmid8180513-
dc.identifier.scopuseid_2-s2.0-0028273140en_US
dc.identifier.volume21en_US
dc.identifier.issue1en_US
dc.identifier.spage62en_US
dc.identifier.epage67en_US
dc.identifier.isiWOS:A1994ND56600010-
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridScottBurden, T=7004306459en_US
dc.identifier.issnl0730-2347-

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