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Article: Endothelium-derived hyperpolarizing factor(s) and the potentiation of kinins by converting enzyme inhibitors

TitleEndothelium-derived hyperpolarizing factor(s) and the potentiation of kinins by converting enzyme inhibitors
Authors
Issue Date1995
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyper
Citation
American Journal Of Hypertension, 1995, v. 8 n. 5 II SUPPL., p. 19S-27S How to Cite?
AbstractInhibitors of angiotensin converting-enzyme (ACE) enhance the endothelium-dependent relaxation to bradykinin and cause the accumulation of kinins in the vascular wall. Bradykinin elicits the production of vasodilator prostanoids and nitric oxide by endothelial cells. However, there is an additional component to the dilator actions of bradykinin, which is mediated by a diffusible endothelium-derived hyperpolarizing factor (EDHF). The knowledge gathered on the nature of EDHF and its mechanism of action are reviewed briefly. EDHF causes hyperpolarization and relaxation of arterial smooth muscle by activating K+-channel, the nature of which varies between species. During the inhibition of both cyclooxygenase and nitric oxide synthase, concentration-response relationships of the hyperpolarization and relaxation elicited by bradykinin overlap in canine coronary arteries. Both effects are enhanced equally by the ACE inhibitor perindoprilat. They are inhibited by membrane depolarization that is obtained by raising the extracellular concentrations of potassium ions. Likewise, in the human coronary artery, the hyperpolarization elicited by bradykinin, which is also mediated by EDHF, is augmented in the presence of perindoprilat and prevented by potassium-induced depolarization. In this blood vessel, contrary to the canine coronary artery, the EDHF-mediated responses occur at concentrations comparable to those initiating the nitric oxide-dependent component. Therefore, the increased production of EDHF, which is induced by kinins, may contribute to the cardiovascular effects of perindoprilat, together with an enhanced production of nitric oxide and vasodilator prostanoids.
Persistent Identifierhttp://hdl.handle.net/10722/171164
ISSN
2015 Impact Factor: 3.182
2015 SCImago Journal Rankings: 1.397
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMombouli, JVen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:12:29Z-
dc.date.available2012-10-30T06:12:29Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Hypertension, 1995, v. 8 n. 5 II SUPPL., p. 19S-27Sen_US
dc.identifier.issn0895-7061en_US
dc.identifier.urihttp://hdl.handle.net/10722/171164-
dc.description.abstractInhibitors of angiotensin converting-enzyme (ACE) enhance the endothelium-dependent relaxation to bradykinin and cause the accumulation of kinins in the vascular wall. Bradykinin elicits the production of vasodilator prostanoids and nitric oxide by endothelial cells. However, there is an additional component to the dilator actions of bradykinin, which is mediated by a diffusible endothelium-derived hyperpolarizing factor (EDHF). The knowledge gathered on the nature of EDHF and its mechanism of action are reviewed briefly. EDHF causes hyperpolarization and relaxation of arterial smooth muscle by activating K+-channel, the nature of which varies between species. During the inhibition of both cyclooxygenase and nitric oxide synthase, concentration-response relationships of the hyperpolarization and relaxation elicited by bradykinin overlap in canine coronary arteries. Both effects are enhanced equally by the ACE inhibitor perindoprilat. They are inhibited by membrane depolarization that is obtained by raising the extracellular concentrations of potassium ions. Likewise, in the human coronary artery, the hyperpolarization elicited by bradykinin, which is also mediated by EDHF, is augmented in the presence of perindoprilat and prevented by potassium-induced depolarization. In this blood vessel, contrary to the canine coronary artery, the EDHF-mediated responses occur at concentrations comparable to those initiating the nitric oxide-dependent component. Therefore, the increased production of EDHF, which is induced by kinins, may contribute to the cardiovascular effects of perindoprilat, together with an enhanced production of nitric oxide and vasodilator prostanoids.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/amjhyperen_US
dc.relation.ispartofAmerican Journal of Hypertensionen_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCoronary Vessels - Metabolismen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEndothelium, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshKinins - Drug Effects - Metabolismen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.titleEndothelium-derived hyperpolarizing factor(s) and the potentiation of kinins by converting enzyme inhibitorsen_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.doi10.1016/0895-7061(95)00029-O-
dc.identifier.pmid7646841-
dc.identifier.scopuseid_2-s2.0-0029005698en_US
dc.identifier.volume8en_US
dc.identifier.issue5 II SUPPL.en_US
dc.identifier.spage19Sen_US
dc.identifier.epage27Sen_US
dc.identifier.isiWOS:A1995RB67900004-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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