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- Publisher Website: 10.1016/j.pharmthera.2009.02.006
- Scopus: eid_2-s2.0-64249116669
- PMID: 19285526
- WOS: WOS:000266030600005
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Article: Prostanoids and reactive oxygen species: Team players in endothelium-dependent contractions
Title | Prostanoids and reactive oxygen species: Team players in endothelium-dependent contractions |
---|---|
Authors | |
Keywords | EDCF Endothelium-dependent contraction Endothelium-derived contracting factor Prostacyclin Reactive oxygen species Thromboxane A2 |
Issue Date | 2009 |
Publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/pharmthera |
Citation | Pharmacology And Therapeutics, 2009, v. 122 n. 2, p. 140-149 How to Cite? |
Abstract | The endothelial cells control the tone of the underlying vascular smooth muscle by releasing vasoactive substances. Endothelium-derived relaxing factors (EDRF), in particular nitric oxide have received considerable attention, but much less is known about the ability of the endothelial cells to release endothelium-derived contracting factors (EDCF). The possible players of endothelium-dependent contractions and the underlying mechanisms leading to the release of EDCF will be discussed in the present review. EDCF is likely to consist of two components: 1) prostanoids (including endoperoxides, prostacyclin, thromboxane A2, and prostaglandin E2) and 2) reactive oxygen species. The former directly activate thromboxane/prostaglandin endoperoxide (TP) receptors of the vascular smooth muscle cells which leads to their contraction, while the latter first stimulate the cyclooxygenase in the smooth muscle with subsequent stimulation of the TP receptors by the prostanoids produced. Dysfunction in calcium handling is the leading causal factor for the exacerbated occurrence of endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat (SHR). The observed increased expressions of endothelial COX-1, prostacyclin synthase, thromboxane synthase and enhanced TP receptor sensitivity are not prerequisites for, but intensify the magnitude of endothelium-dependent contractions. Selective TP receptor antagonists are effective in preventing endothelium-dependent contractions in vitro which highlights the prospective use of such drugs in correcting the imbalanced release of endothelium-derived vasoactive substances that accompany vascular disease. © 2009 Elsevier Inc. All rights reserved. |
Persistent Identifier | http://hdl.handle.net/10722/59543 |
ISSN | 2023 Impact Factor: 12.0 2023 SCImago Journal Rankings: 3.150 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tang, EHC | en_HK |
dc.contributor.author | Vanhoutte, PM | en_HK |
dc.date.accessioned | 2010-05-31T03:52:24Z | - |
dc.date.available | 2010-05-31T03:52:24Z | - |
dc.date.issued | 2009 | en_HK |
dc.identifier.citation | Pharmacology And Therapeutics, 2009, v. 122 n. 2, p. 140-149 | en_HK |
dc.identifier.issn | 0163-7258 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/59543 | - |
dc.description.abstract | The endothelial cells control the tone of the underlying vascular smooth muscle by releasing vasoactive substances. Endothelium-derived relaxing factors (EDRF), in particular nitric oxide have received considerable attention, but much less is known about the ability of the endothelial cells to release endothelium-derived contracting factors (EDCF). The possible players of endothelium-dependent contractions and the underlying mechanisms leading to the release of EDCF will be discussed in the present review. EDCF is likely to consist of two components: 1) prostanoids (including endoperoxides, prostacyclin, thromboxane A2, and prostaglandin E2) and 2) reactive oxygen species. The former directly activate thromboxane/prostaglandin endoperoxide (TP) receptors of the vascular smooth muscle cells which leads to their contraction, while the latter first stimulate the cyclooxygenase in the smooth muscle with subsequent stimulation of the TP receptors by the prostanoids produced. Dysfunction in calcium handling is the leading causal factor for the exacerbated occurrence of endothelium-dependent contractions in the aorta of the spontaneously hypertensive rat (SHR). The observed increased expressions of endothelial COX-1, prostacyclin synthase, thromboxane synthase and enhanced TP receptor sensitivity are not prerequisites for, but intensify the magnitude of endothelium-dependent contractions. Selective TP receptor antagonists are effective in preventing endothelium-dependent contractions in vitro which highlights the prospective use of such drugs in correcting the imbalanced release of endothelium-derived vasoactive substances that accompany vascular disease. © 2009 Elsevier Inc. All rights reserved. | en_HK |
dc.language | eng | en_HK |
dc.publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/pharmthera | en_HK |
dc.relation.ispartof | Pharmacology and Therapeutics | en_HK |
dc.subject | EDCF | en_HK |
dc.subject | Endothelium-dependent contraction | en_HK |
dc.subject | Endothelium-derived contracting factor | en_HK |
dc.subject | Prostacyclin | en_HK |
dc.subject | Reactive oxygen species | en_HK |
dc.subject | Thromboxane A2 | en_HK |
dc.subject.mesh | Endothelium, Vascular - physiology | - |
dc.subject.mesh | Muscle Contraction - physiology | - |
dc.subject.mesh | Muscle, Smooth, Vascular - physiology | - |
dc.subject.mesh | Prostaglandins - physiology | - |
dc.subject.mesh | Reactive Oxygen Species - metabolism | - |
dc.title | Prostanoids and reactive oxygen species: Team players in endothelium-dependent contractions | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0163-7258&volume=122&issue=2&spage=140&epage=149&date=2009&atitle=Prostanoids+and+reactive+oxygen+species:+Team+players+in+endothelium-dependent+contractions | en_HK |
dc.identifier.email | Tang, EHC: evatang1@hku.hk | en_HK |
dc.identifier.email | Vanhoutte, PM: vanhoutt@hku.hk | en_HK |
dc.identifier.authority | Tang, EHC=rp01382 | en_HK |
dc.identifier.authority | Vanhoutte, PM=rp00238 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.pharmthera.2009.02.006 | en_HK |
dc.identifier.pmid | 19285526 | - |
dc.identifier.scopus | eid_2-s2.0-64249116669 | en_HK |
dc.identifier.hkuros | 166649 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-64249116669&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 122 | en_HK |
dc.identifier.issue | 2 | en_HK |
dc.identifier.spage | 140 | en_HK |
dc.identifier.epage | 149 | en_HK |
dc.identifier.eissn | 1879-016X | - |
dc.identifier.isi | WOS:000266030600005 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Tang, EHC=9536518500 | en_HK |
dc.identifier.scopusauthorid | Vanhoutte, PM=7202304247 | en_HK |
dc.identifier.citeulike | 5127088 | - |
dc.identifier.issnl | 0163-7258 | - |