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Conference Paper: Endothelium-dependent effects of converting-enzyme inhibitors

TitleEndothelium-dependent effects of converting-enzyme inhibitors
Authors
Issue Date1993
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/
Citation
Journal Of Cardiovascular Pharmacology, 1993, v. 22 SUPPL. 5, p. S10-S16 How to Cite?
AbstractAngiotensin-converting enzyme (ACE) inhibitors were designed to prevent the vasoconstrictor influence of the activated renin-angiotensin system. However, it has long been suspected that the vasodilator actions of these compounds are not entirely related to inhibition of the generation of angiotensin II. Bradykinin, which is rapidly degraded by ACE, stimulates the release of endothelium-derived vasodilator mediators, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin. These mediators do not contribute to the vasodilator effect of bradykinin in every arterial bed. However, the prevention by ACE inhibitors of the degradation of bradykinin-induces an augmentation of the production of these substances and thus potentiates the dilatation evoked by the peptide. The existence of a local kallikrein-kinin system in the vascular wall has been demonstrated, and locally generated kinins contribute to the acute vasodilator actions of ACE inhibitors. ACE inhibitors can potentiate endothelium-dependent dilatations evoked by neurohumoral mediators that are not substrates for ACE. Thus, the vasodilator properties of ACE inhibitors not only reflect inhibition of the renin-angiotensin system but also depend on the enhanced production of endothelium-derived mediators.
Persistent Identifierhttp://hdl.handle.net/10722/173512
ISSN
2015 Impact Factor: 2.462
2015 SCImago Journal Rankings: 0.962
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorIlliano, SCen_US
dc.contributor.authorNagao, Ten_US
dc.contributor.authorVidal, Men_US
dc.contributor.authorMombouli , JVen_US
dc.date.accessioned2012-10-30T06:32:27Z-
dc.date.available2012-10-30T06:32:27Z-
dc.date.issued1993en_US
dc.identifier.citationJournal Of Cardiovascular Pharmacology, 1993, v. 22 SUPPL. 5, p. S10-S16en_US
dc.identifier.issn0160-2446en_US
dc.identifier.urihttp://hdl.handle.net/10722/173512-
dc.description.abstractAngiotensin-converting enzyme (ACE) inhibitors were designed to prevent the vasoconstrictor influence of the activated renin-angiotensin system. However, it has long been suspected that the vasodilator actions of these compounds are not entirely related to inhibition of the generation of angiotensin II. Bradykinin, which is rapidly degraded by ACE, stimulates the release of endothelium-derived vasodilator mediators, including nitric oxide, endothelium-derived hyperpolarizing factor, and prostacyclin. These mediators do not contribute to the vasodilator effect of bradykinin in every arterial bed. However, the prevention by ACE inhibitors of the degradation of bradykinin-induces an augmentation of the production of these substances and thus potentiates the dilatation evoked by the peptide. The existence of a local kallikrein-kinin system in the vascular wall has been demonstrated, and locally generated kinins contribute to the acute vasodilator actions of ACE inhibitors. ACE inhibitors can potentiate endothelium-dependent dilatations evoked by neurohumoral mediators that are not substrates for ACE. Thus, the vasodilator properties of ACE inhibitors not only reflect inhibition of the renin-angiotensin system but also depend on the enhanced production of endothelium-derived mediators.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.cardiovascularpharm.com/en_US
dc.relation.ispartofJournal of Cardiovascular Pharmacologyen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlood Vessels - Metabolismen_US
dc.subject.meshBradykinin - Metabolism - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshHypertension - Drug Therapyen_US
dc.subject.meshKallikreins - Metabolismen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effectsen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleEndothelium-dependent effects of converting-enzyme inhibitorsen_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.doi10.1097/00005344-199322005-00003-
dc.identifier.pmid7508046-
dc.identifier.scopuseid_2-s2.0-0027381860en_US
dc.identifier.volume22en_US
dc.identifier.issueSUPPL. 5en_US
dc.identifier.spageS10en_US
dc.identifier.epageS16en_US
dc.identifier.isiWOS:A1993MF17900003-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridIlliano, SC=6602119848en_US
dc.identifier.scopusauthoridNagao, T=7401489430en_US
dc.identifier.scopusauthoridVidal, M=7202764932en_US
dc.identifier.scopusauthoridMombouli , JV=7004285772en_US

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