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Article: Prostanoids and reactive oxygen species: Team players in endothelium-dependent contractions

TitleProstanoids and reactive oxygen species: Team players in endothelium-dependent contractions
Authors
KeywordsEDCF
Endothelium-dependent contraction
Endothelium-derived contracting factor
Prostacyclin
Reactive oxygen species
Thromboxane A2
Issue Date2009
PublisherElsevier 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?
AbstractThe 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 Identifierhttp://hdl.handle.net/10722/59543
ISSN
2015 Impact Factor: 11.0
2015 SCImago Journal Rankings: 4.090
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTang, EHCen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-05-31T03:52:24Z-
dc.date.available2010-05-31T03:52:24Z-
dc.date.issued2009en_HK
dc.identifier.citationPharmacology And Therapeutics, 2009, v. 122 n. 2, p. 140-149en_HK
dc.identifier.issn0163-7258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59543-
dc.description.abstractThe 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.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/pharmtheraen_HK
dc.relation.ispartofPharmacology and Therapeuticsen_HK
dc.subjectEDCFen_HK
dc.subjectEndothelium-dependent contractionen_HK
dc.subjectEndothelium-derived contracting factoren_HK
dc.subjectProstacyclinen_HK
dc.subjectReactive oxygen speciesen_HK
dc.subjectThromboxane A2en_HK
dc.subject.meshEndothelium, Vascular - physiology-
dc.subject.meshMuscle Contraction - physiology-
dc.subject.meshMuscle, Smooth, Vascular - physiology-
dc.subject.meshProstaglandins - physiology-
dc.subject.meshReactive Oxygen Species - metabolism-
dc.titleProstanoids and reactive oxygen species: Team players in endothelium-dependent contractionsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://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+contractionsen_HK
dc.identifier.emailTang, EHC: evatang1@hku.hken_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityTang, EHC=rp01382en_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.pharmthera.2009.02.006en_HK
dc.identifier.pmid19285526-
dc.identifier.scopuseid_2-s2.0-64249116669en_HK
dc.identifier.hkuros166649en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-64249116669&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume122en_HK
dc.identifier.issue2en_HK
dc.identifier.spage140en_HK
dc.identifier.epage149en_HK
dc.identifier.eissn1879-016X-
dc.identifier.isiWOS:000266030600005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTang, EHC=9536518500en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike5127088-

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