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Article: EDHF: An update

TitleEDHF: An update
Authors
KeywordsCell membrane
Endothelium
Endothelium-derived hyperpolarizing factor (EDHF)
Myoendothelial gap junction
Potassium channel
Potential
Issue Date2009
PublisherPortland Press Ltd. The Journal's web site is located at http://www.clinsci.org/
Citation
Clinical Science, 2009, v. 117 n. 4, p. 139-155 How to Cite?
AbstractThe endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term 'endothelium-derived hyperpolarizing factor' (EDHF). However, this acronym includes different mechanisms. Arachidonic acid metabolites derived from the cyclo-oxygenases, lipoxygenases and cytochrome P450 pathways, H 2O 2, CO, H 2S and various peptides can be released by endothelial cells. These factors activate different families of K + channels and hyperpolarization of the vascular smooth muscle cells contribute to the mechanisms leading to their relaxation. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca 2+ concentration of the endothelial cells, followed by the opening of SK Ca and IK Ca channels (small and intermediate conductance Ca 2+-activated K + channels respectively). These channels have a distinct subcellular distribution: SK Ca are widely distributed over the plasma membrane, whereas IK Ca are preferentially expressed in the endothelial projections toward the smooth muscle cells. Following SK Ca activation, smooth muscle hyperpolarization is preferentially evoked by electrical coupling through myoendothelial gap junctions, whereas, following IK Ca activation, K + efflux can activate smooth muscle Kir2.1 and/or Na +/ K +-ATPase. EDHF-mediated responses are altered by aging and various pathologies. Therapeutic interventions can restore these responses, suggesting that the improvement in the EDHF pathway contributes to their beneficial effect. A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases. © The Authors Journal compilation © 2009 Biochemical Society.
Persistent Identifierhttp://hdl.handle.net/10722/80191
ISSN
2015 Impact Factor: 4.996
2015 SCImago Journal Rankings: 2.427
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorVanHoutte, PMen_HK
dc.date.accessioned2010-09-06T08:03:31Z-
dc.date.available2010-09-06T08:03:31Z-
dc.date.issued2009en_HK
dc.identifier.citationClinical Science, 2009, v. 117 n. 4, p. 139-155en_HK
dc.identifier.issn0143-5221en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80191-
dc.description.abstractThe endothelium controls vascular tone not only by releasing NO and prostacyclin, but also by other pathways causing hyperpolarization of the underlying smooth muscle cells. This characteristic was at the origin of the term 'endothelium-derived hyperpolarizing factor' (EDHF). However, this acronym includes different mechanisms. Arachidonic acid metabolites derived from the cyclo-oxygenases, lipoxygenases and cytochrome P450 pathways, H 2O 2, CO, H 2S and various peptides can be released by endothelial cells. These factors activate different families of K + channels and hyperpolarization of the vascular smooth muscle cells contribute to the mechanisms leading to their relaxation. Additionally, another pathway associated with the hyperpolarization of both endothelial and vascular smooth muscle cells contributes also to endothelium-dependent relaxations (EDHF-mediated responses). These responses involve an increase in the intracellular Ca 2+ concentration of the endothelial cells, followed by the opening of SK Ca and IK Ca channels (small and intermediate conductance Ca 2+-activated K + channels respectively). These channels have a distinct subcellular distribution: SK Ca are widely distributed over the plasma membrane, whereas IK Ca are preferentially expressed in the endothelial projections toward the smooth muscle cells. Following SK Ca activation, smooth muscle hyperpolarization is preferentially evoked by electrical coupling through myoendothelial gap junctions, whereas, following IK Ca activation, K + efflux can activate smooth muscle Kir2.1 and/or Na +/ K +-ATPase. EDHF-mediated responses are altered by aging and various pathologies. Therapeutic interventions can restore these responses, suggesting that the improvement in the EDHF pathway contributes to their beneficial effect. A better characterization of EDHF-mediated responses should allow the determination of whether or not new drugable targets can be identified for the treatment of cardiovascular diseases. © The Authors Journal compilation © 2009 Biochemical Society.en_HK
dc.languageengen_HK
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.clinsci.org/en_HK
dc.relation.ispartofClinical Scienceen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectCell membraneen_HK
dc.subjectEndotheliumen_HK
dc.subjectEndothelium-derived hyperpolarizing factor (EDHF)en_HK
dc.subjectMyoendothelial gap junctionen_HK
dc.subjectPotassium channelen_HK
dc.subjectPotentialen_HK
dc.subject.meshArachidonic Acid - metabolism-
dc.subject.meshBiological Factors - physiology-
dc.subject.meshCardiovascular Diseases - physiopathology-
dc.subject.meshEndothelium, Vascular - metabolism - physiology - physiopathology-
dc.subject.meshHumans-
dc.titleEDHF: An updateen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-5221&volume=117&issue=4&spage=139&epage=155&date=2009&atitle=EDHF:+an+upadateen_HK
dc.identifier.emailVanHoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanHoutte, PM=rp00238en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1042/CS20090096en_HK
dc.identifier.pmid19601928-
dc.identifier.scopuseid_2-s2.0-70349397556en_HK
dc.identifier.hkuros169810en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70349397556&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume117en_HK
dc.identifier.issue4en_HK
dc.identifier.spage139en_HK
dc.identifier.epage155en_HK
dc.identifier.isiWOS:000268647500005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridVanHoutte, PM=7202304247en_HK

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