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Article: Endothelium-dependent hyperpolarizations: Past beliefs and present facts

TitleEndothelium-dependent hyperpolarizations: Past beliefs and present facts
Authors
KeywordsCardiovascular diseases
Cell membrane potential
EDHF
Endothelial dysfunction
Endothelium
Myoendothelial gap junctions
Potassium channels
Issue Date2007
PublisherTaylor & Francis A B. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/07853890.html
Citation
Annals Of Medicine, 2007, v. 39 n. 7, p. 495-516 How to Cite?
AbstractEndothelium-dependent relaxations are attributed to the release of various factors, such as nitric oxide, carbon monoxide, reactive oxygen species, adenosine, peptides and arachidonic acid metabolites derived from the cyclooxygenases, lipoxygenases, and cytochrome P450 monooxygenases pathways. The hyperpolarization of the smooth muscle cell can contribute to or be an integral part of the mechanisms underlying the relaxations elicited by virtually all these endothelial mediators. These endothelium-derived factors can activate different families of K+ channels of the vascular smooth muscle. Other events associated with the hyperpolarization of both the endothelial and the vascular smooth muscle cells (endothelium-derived hyperpolarizing factor (EDHF)-mediated responses) contribute also to endothelium-dependent relaxations. These responses involve an increase in the intracellular Ca2+ concentration of the endothelial cells followed by the opening of Ca2+-activated K+ channels of small and intermediate conductance and the subsequent hyperpolarization of these cells. Then, the endothelium-dependent hyperpolarization of the underlying smooth muscle cells can be evoked by direct electrical coupling through myoendothelial junctions and/or the accumulation of K+ ions in the intercellular space between the two cell types. These various mechanisms are not necessarily mutually exclusive and, depending on the vascular bed and the experimental conditions, can occur simultaneously or sequentially, or also may act synergistically. © 2007 Taylor & Francis.
Persistent Identifierhttp://hdl.handle.net/10722/80315
ISSN
2015 Impact Factor: 3.763
2015 SCImago Journal Rankings: 1.658
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-09-06T08:04:57Z-
dc.date.available2010-09-06T08:04:57Z-
dc.date.issued2007en_HK
dc.identifier.citationAnnals Of Medicine, 2007, v. 39 n. 7, p. 495-516en_HK
dc.identifier.issn0785-3890en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80315-
dc.description.abstractEndothelium-dependent relaxations are attributed to the release of various factors, such as nitric oxide, carbon monoxide, reactive oxygen species, adenosine, peptides and arachidonic acid metabolites derived from the cyclooxygenases, lipoxygenases, and cytochrome P450 monooxygenases pathways. The hyperpolarization of the smooth muscle cell can contribute to or be an integral part of the mechanisms underlying the relaxations elicited by virtually all these endothelial mediators. These endothelium-derived factors can activate different families of K+ channels of the vascular smooth muscle. Other events associated with the hyperpolarization of both the endothelial and the vascular smooth muscle cells (endothelium-derived hyperpolarizing factor (EDHF)-mediated responses) contribute also to endothelium-dependent relaxations. These responses involve an increase in the intracellular Ca2+ concentration of the endothelial cells followed by the opening of Ca2+-activated K+ channels of small and intermediate conductance and the subsequent hyperpolarization of these cells. Then, the endothelium-dependent hyperpolarization of the underlying smooth muscle cells can be evoked by direct electrical coupling through myoendothelial junctions and/or the accumulation of K+ ions in the intercellular space between the two cell types. These various mechanisms are not necessarily mutually exclusive and, depending on the vascular bed and the experimental conditions, can occur simultaneously or sequentially, or also may act synergistically. © 2007 Taylor & Francis.en_HK
dc.languageengen_HK
dc.publisherTaylor & Francis A B. The Journal's web site is located at http://www.tandf.co.uk/journals/titles/07853890.htmlen_HK
dc.relation.ispartofAnnals of Medicineen_HK
dc.subjectCardiovascular diseasesen_HK
dc.subjectCell membrane potentialen_HK
dc.subjectEDHFen_HK
dc.subjectEndothelial dysfunctionen_HK
dc.subjectEndotheliumen_HK
dc.subjectMyoendothelial gap junctionsen_HK
dc.subjectPotassium channelsen_HK
dc.titleEndothelium-dependent hyperpolarizations: Past beliefs and present factsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0785-3890&volume=39&spage=495&epage=519&date=2007&atitle=Endothelium-dependent+hyperpolarizations:+Past+beliefs+and+present+factsen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1080/07853890701491000en_HK
dc.identifier.pmid17852039-
dc.identifier.scopuseid_2-s2.0-35748931462en_HK
dc.identifier.hkuros151852en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-35748931462&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume39en_HK
dc.identifier.issue7en_HK
dc.identifier.spage495en_HK
dc.identifier.epage516en_HK
dc.identifier.isiWOS:000251046500002-
dc.publisher.placeSwedenen_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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