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- Publisher Website: 10.1038/aps.2010.127
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- PMID: 20711228
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Article: COX-mediated endothelium-dependent contractions: From the past to recent discoveries
Title | COX-mediated endothelium-dependent contractions: From the past to recent discoveries |
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Authors | |
Keywords | cyclooxygenase EDCF endothelium gap junctions phospholipase A2 prostanoids reactive oxygen species TP-receptors |
Issue Date | 2010 |
Publisher | Nature 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? |
Abstract | Endothelial 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 Identifier | http://hdl.handle.net/10722/125260 |
ISSN | 2023 Impact Factor: 6.9 2023 SCImago Journal Rankings: 1.882 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Wong, MSK | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.date.accessioned | 2010-10-31T11:20:35Z | - |
dc.date.available | 2010-10-31T11:20:35Z | - |
dc.date.issued | 2010 | en_HK |
dc.identifier.citation | Acta Pharmacologica Sinica, 2010, v. 31 n. 9, p. 1095-1102 | en_HK |
dc.identifier.issn | 1671-4083 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/125260 | - |
dc.description.abstract | Endothelial 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.language | eng | en_HK |
dc.publisher | Nature Publishing Group. The Journal's web site is located at http://www.nature.com/aps/index.html | en_HK |
dc.relation.ispartof | Acta Pharmacologica Sinica | en_HK |
dc.subject | cyclooxygenase | en_HK |
dc.subject | EDCF | en_HK |
dc.subject | endothelium | en_HK |
dc.subject | gap junctions | en_HK |
dc.subject | phospholipase A2 | en_HK |
dc.subject | prostanoids | en_HK |
dc.subject | reactive oxygen species | en_HK |
dc.subject | TP-receptors | en_HK |
dc.subject.mesh | Arachidonic Acid - metabolism | - |
dc.subject.mesh | Endothelial Cells - metabolism - pathology | - |
dc.subject.mesh | Phospholipases A2 - metabolism | - |
dc.subject.mesh | Prostaglandin-Endoperoxide Synthases - metabolism | - |
dc.subject.mesh | Vasoconstrictor Agents - metabolism | - |
dc.title | COX-mediated endothelium-dependent contractions: From the past to recent discoveries | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+discoveries | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.description.nature | postprint | - |
dc.identifier.doi | 10.1038/aps.2010.127 | en_HK |
dc.identifier.pmid | 20711228 | - |
dc.identifier.scopus | eid_2-s2.0-77956358848 | en_HK |
dc.identifier.hkuros | 182813 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-77956358848&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 31 | en_HK |
dc.identifier.issue | 9 | en_HK |
dc.identifier.spage | 1095 | en_HK |
dc.identifier.epage | 1102 | en_HK |
dc.identifier.isi | WOS:000281562900014 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Wong, MSK=23483301500 | en_HK |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_HK |
dc.identifier.issnl | 1671-4083 | - |