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Conference Paper: Endothelial dysfunction and inhibition of converting enzyme

TitleEndothelial dysfunction and inhibition of converting enzyme
Authors
Issue Date1998
PublisherOxford University Press. The Journal's web site is located at http://eurheartj.oxfordjournals.org/
Citation
European Heart Journal, 1998, v. 19 SUPPL. J, p. J7-J15 How to Cite?
AbstractEndothelial cells control the tone of the underlying vascular smooth muscle by secreting vasodilator substances (prostacyclin, nitric oxide and endothelium-derived hyperpolarizing factor). These vasodilator substances also contribute to the antithrombogenicity of the normal endothelium, and inhibit cellular growth. In coronary vascular disease, the ability of the endothelium to secrete vasodilator substances is reduced, while the propensity to release endothelium-derived contracting factors is increased. In particular, the reduced release of nitric oxide in response to aggregating platelets, thrombin and circulating catecholamines favours the occurrence of thrombosis and vasospasm, and plays a key role in the initiation of the atherosclerotic process. From the therapeutic point of view, the best available way to enhance the release of endothelium-derived nitric oxide and hyperpolarizing factor is to inhibit converting enzyme. This will protect endogenous bradykinin from breakdown and prolong its action on endothelial receptors.
Persistent Identifierhttp://hdl.handle.net/10722/173532
ISSN
2015 Impact Factor: 15.064
2015 SCImago Journal Rankings: 6.997
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:32Z-
dc.date.available2012-10-30T06:32:32Z-
dc.date.issued1998en_US
dc.identifier.citationEuropean Heart Journal, 1998, v. 19 SUPPL. J, p. J7-J15en_US
dc.identifier.issn0195-668Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/173532-
dc.description.abstractEndothelial cells control the tone of the underlying vascular smooth muscle by secreting vasodilator substances (prostacyclin, nitric oxide and endothelium-derived hyperpolarizing factor). These vasodilator substances also contribute to the antithrombogenicity of the normal endothelium, and inhibit cellular growth. In coronary vascular disease, the ability of the endothelium to secrete vasodilator substances is reduced, while the propensity to release endothelium-derived contracting factors is increased. In particular, the reduced release of nitric oxide in response to aggregating platelets, thrombin and circulating catecholamines favours the occurrence of thrombosis and vasospasm, and plays a key role in the initiation of the atherosclerotic process. From the therapeutic point of view, the best available way to enhance the release of endothelium-derived nitric oxide and hyperpolarizing factor is to inhibit converting enzyme. This will protect endogenous bradykinin from breakdown and prolong its action on endothelial receptors.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://eurheartj.oxfordjournals.org/en_US
dc.relation.ispartofEuropean Heart Journalen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacology - Therapeutic Useen_US
dc.subject.meshBradykinin - Drug Effects - Metabolismen_US
dc.subject.meshCoronary Disease - Drug Therapy - Etiology - Metabolismen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Secretionen_US
dc.subject.meshHumansen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshPeptidyl-Dipeptidase A - Metabolismen_US
dc.subject.meshPrognosisen_US
dc.titleEndothelial dysfunction and inhibition of converting enzymeen_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.pmid9796835-
dc.identifier.scopuseid_2-s2.0-0031713430en_US
dc.identifier.volume19en_US
dc.identifier.issueSUPPL. Jen_US
dc.identifier.spageJ7en_US
dc.identifier.epageJ15en_US
dc.identifier.isiWOS:000076071700003-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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