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Conference Paper: Endothelium-derived relaxing factors and converting enzyme inhibition

TitleEndothelium-derived relaxing factors and converting enzyme inhibition
Authors
Issue Date1995
PublisherExcerpta Medica, Inc.. The Journal's web site is located at http://www.ajconline.org/
Citation
American Journal Of Cardiology, 1995, v. 76 n. 15, p. 3E-12E How to Cite?
AbstractEndothelial cells can produce at least 3 substances which cause relaxation of vascular smooth muscle: (1) endothelium-derived nitric oxide (NO, which is secreted not only toward the underlying vascular smooth muscle but also into the blood vessel lumen). NO also has a physiological role at the interface between the endothelial cells and the blood content; in particular, NO inhibits the adhesion of platelets and leukocytes to the endothelium. (2) Endothelium-derived hyperpolarizing factor, presumably a labile metabolite of arachidonic acid formed through the P-450 pathway, which appears to act on smooth muscle by being one of the few physiologic openers of the potassium channels. (3) Prostacyclin, which can be considered as an endothelium- derived relaxing substance, given its vasodilator activity and its primarily endothelial origin. One of the main factors modulating the release of these EDRFs is the shear stress of blood on the arterial wall, which explains why flow-induced vasodilation is endothelium-dependent in the intact organism. The peptide bradykinin is a potent stimulus for EDRF release. The normal lifespan of an adult human endothelial cell is some 30 years, after which aging takes its toll and the cells must be replaced. The regenerated cells lose some of their ability to release EDRF, in particular in response to platelet aggregation and thrombin. Finally, in hypertension and atherosclerosis, a decrease in endothelium-dependent relaxation is obvious in response to a variety of stimuli. All converting enzyme inhibitors tested so far share a potentiating effect on endothelium-dependent relaxation to bradykinin, and augmented local production of bradykinin may help to explain the acute vasodilator properties of these compounds.
Persistent Identifierhttp://hdl.handle.net/10722/173524
ISSN
2015 Impact Factor: 3.154
2015 SCImago Journal Rankings: 2.063
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBoulanger, CMen_US
dc.contributor.authorMombouli, JVen_US
dc.date.accessioned2012-10-30T06:32:29Z-
dc.date.available2012-10-30T06:32:29Z-
dc.date.issued1995en_US
dc.identifier.citationAmerican Journal Of Cardiology, 1995, v. 76 n. 15, p. 3E-12Een_US
dc.identifier.issn0002-9149en_US
dc.identifier.urihttp://hdl.handle.net/10722/173524-
dc.description.abstractEndothelial cells can produce at least 3 substances which cause relaxation of vascular smooth muscle: (1) endothelium-derived nitric oxide (NO, which is secreted not only toward the underlying vascular smooth muscle but also into the blood vessel lumen). NO also has a physiological role at the interface between the endothelial cells and the blood content; in particular, NO inhibits the adhesion of platelets and leukocytes to the endothelium. (2) Endothelium-derived hyperpolarizing factor, presumably a labile metabolite of arachidonic acid formed through the P-450 pathway, which appears to act on smooth muscle by being one of the few physiologic openers of the potassium channels. (3) Prostacyclin, which can be considered as an endothelium- derived relaxing substance, given its vasodilator activity and its primarily endothelial origin. One of the main factors modulating the release of these EDRFs is the shear stress of blood on the arterial wall, which explains why flow-induced vasodilation is endothelium-dependent in the intact organism. The peptide bradykinin is a potent stimulus for EDRF release. The normal lifespan of an adult human endothelial cell is some 30 years, after which aging takes its toll and the cells must be replaced. The regenerated cells lose some of their ability to release EDRF, in particular in response to platelet aggregation and thrombin. Finally, in hypertension and atherosclerosis, a decrease in endothelium-dependent relaxation is obvious in response to a variety of stimuli. All converting enzyme inhibitors tested so far share a potentiating effect on endothelium-dependent relaxation to bradykinin, and augmented local production of bradykinin may help to explain the acute vasodilator properties of these compounds.en_US
dc.languageengen_US
dc.publisherExcerpta Medica, Inc.. The Journal's web site is located at http://www.ajconline.org/en_US
dc.relation.ispartofAmerican Journal of Cardiologyen_US
dc.subject.meshAdulten_US
dc.subject.meshAngiotensin-Converting Enzyme Inhibitors - Pharmacologyen_US
dc.subject.meshArteriosclerosis - Metabolismen_US
dc.subject.meshBiological Factors - Physiologyen_US
dc.subject.meshBradykinin - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Metabolismen_US
dc.subject.meshEpoprostenol - Physiologyen_US
dc.subject.meshHumansen_US
dc.subject.meshHypertension - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolism - Physiologyen_US
dc.titleEndothelium-derived relaxing factors and converting enzyme inhibitionen_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.doi10.1016/S0002-9149(99)80496-2en_US
dc.identifier.pmid7484885-
dc.identifier.scopuseid_2-s2.0-0028841949en_US
dc.identifier.volume76en_US
dc.identifier.issue15en_US
dc.identifier.spage3Een_US
dc.identifier.epage12Een_US
dc.identifier.isiWOS:A1995TG27100002-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US
dc.identifier.scopusauthoridMombouli, JV=7004285772en_US

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