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Article: Endothelium-dependent contractions in SHR: A tale of prostanoid TP and IP receptors

TitleEndothelium-dependent contractions in SHR: A tale of prostanoid TP and IP receptors
Authors
KeywordsCyclooxygenase
EDCF
Endothelium
Hypertension
Nitric oxide
Oxidative stress
Platelets
Prostaglandins
Smooth muscle
Superoxide anion
Issue Date2009
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, 2009, v. 156 n. 4, p. 563-574 How to Cite?
AbstractIn the aorta of spontaneously hypertensive rats (SHR), the endothelial dysfunction is due to the release of endothelium-derived contracting factors (EDCFs) that counteract the vasodilator effect of nitric oxide, with no or minor alteration of its production. The endothelium-dependent contractions elicited by acetylcholine (ACh) involve an increase in endothelial [Ca 2+] i, the production of reactive oxygen species, the activation of endothelial cyclooxygenase-1, the diffusion of EDCF and the subsequent stimulation of smooth muscle cell TP receptors. The EDCFs released by ACh have been identified as PGH 2 and paradoxically prostacyclin. Prostacyclin generally acts as an endothelium-derived vasodilator, which, by stimulating IP receptors, produces hyperpolarization and relaxation of the smooth muscle and inhibits platelet aggregation. In the aorta of SHR and Wistar-Kyoto rats, prostacyclin is the principal metabolite of arachidonic acid released by ACh. However, in SHR aorta, prostacyclin does not produce relaxations but activates the TP receptors on vascular smooth muscle cells and produces contraction. The IP receptor is not functional in the aortic smooth muscle cells of SHR as early as 12 weeks of age, but its activity is not reduced in platelets. Therefore, prostacyclin in the rule protects the vascular wall, but in the SHR aorta it can contribute to endothelial dysfunction. Whether or not prostacyclin plays a detrimental role as an EDCF in other animal models or in human remains to be demonstrated. Nevertheless, because EDCFs converge to activate TP receptors, selective antagonists of this receptor, by preventing endothelium-dependent contractions, curtail the endothelial dysfunction in diseases such as hypertension and diabetes. © 2009 The British Pharmacological Society.Society.
Persistent Identifierhttp://hdl.handle.net/10722/59538
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorFélétou, Men_HK
dc.contributor.authorVerbeuren, TJen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.date.accessioned2010-05-31T03:52:17Z-
dc.date.available2010-05-31T03:52:17Z-
dc.date.issued2009en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2009, v. 156 n. 4, p. 563-574en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59538-
dc.description.abstractIn the aorta of spontaneously hypertensive rats (SHR), the endothelial dysfunction is due to the release of endothelium-derived contracting factors (EDCFs) that counteract the vasodilator effect of nitric oxide, with no or minor alteration of its production. The endothelium-dependent contractions elicited by acetylcholine (ACh) involve an increase in endothelial [Ca 2+] i, the production of reactive oxygen species, the activation of endothelial cyclooxygenase-1, the diffusion of EDCF and the subsequent stimulation of smooth muscle cell TP receptors. The EDCFs released by ACh have been identified as PGH 2 and paradoxically prostacyclin. Prostacyclin generally acts as an endothelium-derived vasodilator, which, by stimulating IP receptors, produces hyperpolarization and relaxation of the smooth muscle and inhibits platelet aggregation. In the aorta of SHR and Wistar-Kyoto rats, prostacyclin is the principal metabolite of arachidonic acid released by ACh. However, in SHR aorta, prostacyclin does not produce relaxations but activates the TP receptors on vascular smooth muscle cells and produces contraction. The IP receptor is not functional in the aortic smooth muscle cells of SHR as early as 12 weeks of age, but its activity is not reduced in platelets. Therefore, prostacyclin in the rule protects the vascular wall, but in the SHR aorta it can contribute to endothelial dysfunction. Whether or not prostacyclin plays a detrimental role as an EDCF in other animal models or in human remains to be demonstrated. Nevertheless, because EDCFs converge to activate TP receptors, selective antagonists of this receptor, by preventing endothelium-dependent contractions, curtail the endothelial dysfunction in diseases such as hypertension and diabetes. © 2009 The British Pharmacological Society.Society.en_HK
dc.languageengen_HK
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.subjectCyclooxygenaseen_HK
dc.subjectEDCFen_HK
dc.subjectEndotheliumen_HK
dc.subjectHypertensionen_HK
dc.subjectNitric oxideen_HK
dc.subjectOxidative stressen_HK
dc.subjectPlateletsen_HK
dc.subjectProstaglandinsen_HK
dc.subjectSmooth muscleen_HK
dc.subjectSuperoxide anionen_HK
dc.titleEndothelium-dependent contractions in SHR: A tale of prostanoid TP and IP receptorsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=2009;156&spage=563&epage=574&date=2008&atitle=Endothelium-dependent+contractions+in+SHR:+a+tale+of+prostanoid+TP+and+IP+receptorsen_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.1476-5381.2008.00060.xen_HK
dc.identifier.pmid19154435-
dc.identifier.pmcidPMC2697704-
dc.identifier.scopuseid_2-s2.0-65349116560en_HK
dc.identifier.hkuros166700en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-65349116560&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume156en_HK
dc.identifier.issue4en_HK
dc.identifier.spage563en_HK
dc.identifier.epage574en_HK
dc.identifier.isiWOS:000263450000002-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridFélétou, M=7006461826en_HK
dc.identifier.scopusauthoridVerbeuren, TJ=7007006534en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.citeulike8153235-

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