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Article: COX-mediated endothelium-dependent contractions: From the past to recent discoveries

TitleCOX-mediated endothelium-dependent contractions: From the past to recent discoveries
Authors
Keywordscyclooxygenase
EDCF
endothelium
gap junctions
phospholipase A2
prostanoids
reactive oxygen species
TP-receptors
Issue Date2010
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html
Citation
Acta Pharmacologica Sinica, 2010, v. 31 n. 9, p. 1095-1102 How to Cite?
AbstractEndothelial cells release various substances to control the tone of the underlying vascular smooth muscle. Nitric oxide (NO) is the best defined endothelium-derived relaxing factor (EDRF). Endothelial cells can also increase vascular tone by releasing endothelium-derived contracting factors (EDCF). The over-production of EDCF contributes to the endothelial dysfunctions which accompanies various vascular diseases. The present review summarizes and discusses the mechanisms leading to the release of EDCFs derived from the metabolism of arachidonic acid. This release can be triggered by agonists such as acetylcholine, adenosine nucleotides or by stretch. All these stimuli are able to induce calcium influx into the endothelial cells, an effect which can be mimicked by calcium ionophores. The augmentation in intracellular calcium ion concentration initiates the release of EDCF. Downstream processes include activation of phospholipase A 2 (PLA2), cyclooxygenases (COX) and the production of reactive oxygen species (ROS) and vasoconstrictor prostanoids (endoperoxides, prostacyclin, thromboxane A2 and other prostaglandins) which subsequently diffuse to, and activate thromboxane- prostanoid (TP) receptors on the vascular smooth muscle cells leading to contraction. © 2010 CPS and SIMM All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/125260
ISSN
2015 Impact Factor: 3.166
2015 SCImago Journal Rankings: 1.161
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, MSKen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-10-31T11:20:35Z-
dc.date.available2010-10-31T11:20:35Z-
dc.date.issued2010en_HK
dc.identifier.citationActa Pharmacologica Sinica, 2010, v. 31 n. 9, p. 1095-1102en_HK
dc.identifier.issn1671-4083en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125260-
dc.description.abstractEndothelial cells release various substances to control the tone of the underlying vascular smooth muscle. Nitric oxide (NO) is the best defined endothelium-derived relaxing factor (EDRF). Endothelial cells can also increase vascular tone by releasing endothelium-derived contracting factors (EDCF). The over-production of EDCF contributes to the endothelial dysfunctions which accompanies various vascular diseases. The present review summarizes and discusses the mechanisms leading to the release of EDCFs derived from the metabolism of arachidonic acid. This release can be triggered by agonists such as acetylcholine, adenosine nucleotides or by stretch. All these stimuli are able to induce calcium influx into the endothelial cells, an effect which can be mimicked by calcium ionophores. The augmentation in intracellular calcium ion concentration initiates the release of EDCF. Downstream processes include activation of phospholipase A 2 (PLA2), cyclooxygenases (COX) and the production of reactive oxygen species (ROS) and vasoconstrictor prostanoids (endoperoxides, prostacyclin, thromboxane A2 and other prostaglandins) which subsequently diffuse to, and activate thromboxane- prostanoid (TP) receptors on the vascular smooth muscle cells leading to contraction. © 2010 CPS and SIMM All rights reserved.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.htmlen_HK
dc.relation.ispartofActa Pharmacologica Sinicaen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectcyclooxygenaseen_HK
dc.subjectEDCFen_HK
dc.subjectendotheliumen_HK
dc.subjectgap junctionsen_HK
dc.subjectphospholipase A2en_HK
dc.subjectprostanoidsen_HK
dc.subjectreactive oxygen speciesen_HK
dc.subjectTP-receptorsen_HK
dc.subject.meshArachidonic Acid - metabolism-
dc.subject.meshEndothelial Cells - metabolism - pathology-
dc.subject.meshPhospholipases A2 - metabolism-
dc.subject.meshProstaglandin-Endoperoxide Synthases - metabolism-
dc.subject.meshVasoconstrictor Agents - metabolism-
dc.titleCOX-mediated endothelium-dependent contractions: From the past to recent discoveriesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1671-4083&volume=31&issue=9&spage=1095&epage=1102&date=2010&atitle=COX-mediated+endothelium-dependent+contractions:+from+the+past+to+recent+discoveriesen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturepostprint-
dc.identifier.doi10.1038/aps.2010.127en_HK
dc.identifier.pmid20711228-
dc.identifier.scopuseid_2-s2.0-77956358848en_HK
dc.identifier.hkuros182813en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77956358848&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume31en_HK
dc.identifier.issue9en_HK
dc.identifier.spage1095en_HK
dc.identifier.epage1102en_HK
dc.identifier.isiWOS:000281562900014-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, MSK=23483301500en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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