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Article: Endothelium-mediated control of vascular tone: COX-1 and COX-2 products

TitleEndothelium-mediated control of vascular tone: COX-1 and COX-2 products
Authors
Keywordsaging
cyclooxygenases
diabetes
dysfunction
endothelium
hypertension
prostaglandins
Issue Date2011
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 2011, v. 164 n. 3, p. 894-912 How to Cite?
AbstractEndothelium-dependent contractions contribute to endothelial dysfunction in various animal models of aging, diabetes and cardiovascular diseases. In the spontaneously hypertensive rat, the archetypal model for endothelium-dependent contractions, the production of the endothelium-derived contractile factors (EDCF) involves an increase in endothelial intracellular calcium concentration, the production of reactive oxygen species, the predominant activation of cyclooxygenase-1 (COX-1) and to a lesser extent that of COX-2, the diffusion of EDCF towards the smooth muscle cells and the subsequent stimulation of their thromboxane A2-endoperoxide TP receptors. Endothelium-dependent contractions are also observed in various models of hypertension, aging and diabetes. They generally also involve the generation of COX-1- and/or COX-2-derived products and the activation of smooth muscle TP receptors. Depending on the model, thromboxane A 2, PGH 2, PGF 2α, PGE 2 and paradoxically PGI 2 can all act as EDCFs. In human, the production of COX-derived EDCF is a characteristic of the aging and diseased blood vessels, with essential hypertension causing an earlier onset and an acceleration of this endothelial dysfunction. As it has been observed in animal models, COX-1, COX-2 or both isoforms can contribute to these endothelial dysfunctions. Since in most cases, the activation of TP receptors is the common downstream effector, selective antagonists of this receptor should curtail endothelial dysfunction and be of therapeutic interest in the treatment of cardiovascular disorders. © 2011 The British Pharmacological Society.
Persistent Identifierhttp://hdl.handle.net/10722/146895
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong GRF466110
CUHK
Funding Information:

This work is partially supported by Hong Kong GRF (466110) and CUHK Focused Investment Scheme.

References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorHuang, Yen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2012-05-23T05:48:52Z-
dc.date.available2012-05-23T05:48:52Z-
dc.date.issued2011en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2011, v. 164 n. 3, p. 894-912en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/146895-
dc.description.abstractEndothelium-dependent contractions contribute to endothelial dysfunction in various animal models of aging, diabetes and cardiovascular diseases. In the spontaneously hypertensive rat, the archetypal model for endothelium-dependent contractions, the production of the endothelium-derived contractile factors (EDCF) involves an increase in endothelial intracellular calcium concentration, the production of reactive oxygen species, the predominant activation of cyclooxygenase-1 (COX-1) and to a lesser extent that of COX-2, the diffusion of EDCF towards the smooth muscle cells and the subsequent stimulation of their thromboxane A2-endoperoxide TP receptors. Endothelium-dependent contractions are also observed in various models of hypertension, aging and diabetes. They generally also involve the generation of COX-1- and/or COX-2-derived products and the activation of smooth muscle TP receptors. Depending on the model, thromboxane A 2, PGH 2, PGF 2α, PGE 2 and paradoxically PGI 2 can all act as EDCFs. In human, the production of COX-derived EDCF is a characteristic of the aging and diseased blood vessels, with essential hypertension causing an earlier onset and an acceleration of this endothelial dysfunction. As it has been observed in animal models, COX-1, COX-2 or both isoforms can contribute to these endothelial dysfunctions. Since in most cases, the activation of TP receptors is the common downstream effector, selective antagonists of this receptor should curtail endothelial dysfunction and be of therapeutic interest in the treatment of cardiovascular disorders. © 2011 The British Pharmacological Society.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_HK
dc.relation.ispartofBritish Journal of Pharmacologyen_HK
dc.rightsBritish Journal of Pharmacology. Copyright © John Wiley & Sons Ltd.-
dc.subjectagingen_HK
dc.subjectcyclooxygenasesen_HK
dc.subjectdiabetesen_HK
dc.subjectdysfunctionen_HK
dc.subjectendotheliumen_HK
dc.subjecthypertensionen_HK
dc.subjectprostaglandinsen_HK
dc.subject.meshCardiovascular Diseases - enzymology - metabolism - physiopathology-
dc.subject.meshCyclooxygenase 1 - metabolism-
dc.subject.meshCyclooxygenase 2 - metabolism-
dc.subject.meshEndothelins - metabolism-
dc.subject.meshEndothelium, Vascular - enzymology - metabolism - physiology-
dc.titleEndothelium-mediated control of vascular tone: COX-1 and COX-2 productsen_HK
dc.typeArticleen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1111/j.1476-5381.2011.01276.xen_HK
dc.identifier.pmid21323907-
dc.identifier.pmcidPMC3195913-
dc.identifier.scopuseid_2-s2.0-79958056715en_HK
dc.identifier.hkuros199784en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79958056715&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume164en_HK
dc.identifier.issue3en_HK
dc.identifier.spage894en_HK
dc.identifier.epage912en_HK
dc.identifier.isiWOS:000294926000006-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridHuang, Y=34770945300en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK

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