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Article: Endothelium-derived hyperpolarizing factor: Where are we now?

TitleEndothelium-derived hyperpolarizing factor: Where are we now?
Authors
KeywordsCnp
Cyclooxygenase
Cytochrome P450
Edhf
Gap Junction
Lipoxygenase
No
Potassium Channels
Prostacyclin
Issue Date2006
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642
Citation
Arteriosclerosis, Thrombosis, And Vascular Biology, 2006, v. 26 n. 6, p. 1215-1225 How to Cite?
AbstractThe endothelium controls vascular tone not only by releasing nitric oxide (NO) and prostacyclin but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the denomination endothelium-derived hyperpolarizing factor (EDHF). We know now that this acronym includes different mechanisms. In general, EDHF-mediated responses involve an increase in the intracellular calcium concentration, the opening of calcium-activated potassium channels of small and intermediate conductance and the hyperpolarization of the endothelial cells. This results in an endothelium-dependent hyperpolarization of the smooth muscle cells, which can be evoked by direct electrical coupling through myo-endothelial junctions and/or the accumulation of potassium ions in the intercellular space. Potassium ions hyperpolarize the smooth muscle cells by activating inward rectifying potassium channels and/or Na/K-ATPase. In some blood vessels, including large and small coronary arteries, the endothelium releases arachidonic acid metabolites derived from cytochrome P450 monooxygenases. The epoxyeicosatrienoic acids (EET) generated are not only intracellular messengers but also can diffuse and hyperpolarize the smooth muscle cells by activating large conductance calcium-activated potassium channels. Additionally, the endothelium can produce other factors such as lipoxygenases derivatives or hydrogen peroxide (H2O2). These different mechanisms are not necessarily exclusive and can occur simultaneously. © 2006 American Heart Association, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/171342
ISSN
2015 Impact Factor: 5.969
2015 SCImago Journal Rankings: 3.356
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:29Z-
dc.date.available2012-10-30T06:13:29Z-
dc.date.issued2006en_US
dc.identifier.citationArteriosclerosis, Thrombosis, And Vascular Biology, 2006, v. 26 n. 6, p. 1215-1225en_US
dc.identifier.issn1079-5642en_US
dc.identifier.urihttp://hdl.handle.net/10722/171342-
dc.description.abstractThe endothelium controls vascular tone not only by releasing nitric oxide (NO) and prostacyclin but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the denomination endothelium-derived hyperpolarizing factor (EDHF). We know now that this acronym includes different mechanisms. In general, EDHF-mediated responses involve an increase in the intracellular calcium concentration, the opening of calcium-activated potassium channels of small and intermediate conductance and the hyperpolarization of the endothelial cells. This results in an endothelium-dependent hyperpolarization of the smooth muscle cells, which can be evoked by direct electrical coupling through myo-endothelial junctions and/or the accumulation of potassium ions in the intercellular space. Potassium ions hyperpolarize the smooth muscle cells by activating inward rectifying potassium channels and/or Na/K-ATPase. In some blood vessels, including large and small coronary arteries, the endothelium releases arachidonic acid metabolites derived from cytochrome P450 monooxygenases. The epoxyeicosatrienoic acids (EET) generated are not only intracellular messengers but also can diffuse and hyperpolarize the smooth muscle cells by activating large conductance calcium-activated potassium channels. Additionally, the endothelium can produce other factors such as lipoxygenases derivatives or hydrogen peroxide (H2O2). These different mechanisms are not necessarily exclusive and can occur simultaneously. © 2006 American Heart Association, Inc.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.lww.com/product/?1079-5642en_US
dc.relation.ispartofArteriosclerosis, Thrombosis, and Vascular Biologyen_US
dc.rightsArteriosclerosis, Thrombosis, and Vascular Biology. Copyright © Lippincott Williams & Wilkins.-
dc.subjectCnpen_US
dc.subjectCyclooxygenaseen_US
dc.subjectCytochrome P450en_US
dc.subjectEdhfen_US
dc.subjectGap Junctionen_US
dc.subjectLipoxygenaseen_US
dc.subjectNoen_US
dc.subjectPotassium Channelsen_US
dc.subjectProstacyclinen_US
dc.titleEndothelium-derived hyperpolarizing factor: Where are we now?en_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.doi10.1161/01.ATV.0000217611.81085.c5en_US
dc.identifier.scopuseid_2-s2.0-33745023668en_US
dc.identifier.hkuros119618-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745023668&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume26en_US
dc.identifier.issue6en_US
dc.identifier.spage1215en_US
dc.identifier.epage1225en_US
dc.identifier.isiWOS:000237644000008-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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