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Article: Acetylcholine-induced endothelium-dependent contractions in the SHR aorta: The Janus face of prostacyclin

TitleAcetylcholine-induced endothelium-dependent contractions in the SHR aorta: The Janus face of prostacyclin
Authors
KeywordsEndoperoxide
Endothelium-dependent contractions
Prostacyclin
Prostaglandins
Spontaneously hypertensive rat
TP receptors
Issue Date2005
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, 2005, v. 146 n. 6, p. 834-845 How to Cite?
Abstract1 In the spontaneously hypertensive rat (SHR) and aging Wistar-Kyoto rats (WKY), acetylcholine releases an endothelium-derived contracting factor (EDCF) produced by endothelial cyclooxygenase-1, which stimulates thromboxane A 2 receptors (TP receptors) on vascular smooth muscle. The purpose of the present study was to identify this EDCF by measuring changes in isometric tension and the release of various prostaglandins by acetylcholine. 2 In isolated aortic rings of SHR, U 46619, prostaglandin (PG) H 2, PGF 2α, PGE 2, PGD 2, prostacyclin (PGI 2) and 8-isoprostane, all activate TP receptors of the vascular smooth muscle to produce a contraction (U 46619≫8-isoprostane=PGF 2α=PGH 2>PGE 2=PGD 2> PGI 2). The contractions produced by PGH 2 and PGI 2 were fast and transient, mimicking endothelium-dependent contractions. PGI 2 did not relax isolated aortic rings of WKY and SHR. 3 Acetylcholine evoked the endothelium-dependent release of thromboxane A 2, PGF 2α, PGE 2, PGI 2 and most likely PGH 2 (PGI 2≫PGF 2α≥PGE 2>TXA 2>8-isoprostane, PGD 2). Dazoxiben abolished the production of thromboxane A 2, but did not influence the endothelium-dependent contractions to acetylcholine. 4 The release of PGI 2 was significantly larger in the aorta of SHR than in WKY, and the former was more sensitive to the contractile effect of PGI 2 than the latter. The inhibition of PGI-synthase was associated with an increase in PGH 2 spillover and the enhancement of acetylcholine-induced endothelium-dependent contractions. 5 Thus, in the aorta of SHR and aging WKY, the endothelium-dependent contractions elicited by acetylcholine most likely involve the release of PGI 2 with a concomitant contribution of PGH 2. © 2005 Nature Publishing Group All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/49271
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGluais, Pen_HK
dc.contributor.authorLonchampt, Men_HK
dc.contributor.authorMorrow, JDen_HK
dc.contributor.authorVanhoutte, PMen_HK
dc.contributor.authorFeletou, Men_HK
dc.date.accessioned2008-06-12T06:38:10Z-
dc.date.available2008-06-12T06:38:10Z-
dc.date.issued2005en_HK
dc.identifier.citationBritish Journal Of Pharmacology, 2005, v. 146 n. 6, p. 834-845en_HK
dc.identifier.issn0007-1188en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49271-
dc.description.abstract1 In the spontaneously hypertensive rat (SHR) and aging Wistar-Kyoto rats (WKY), acetylcholine releases an endothelium-derived contracting factor (EDCF) produced by endothelial cyclooxygenase-1, which stimulates thromboxane A 2 receptors (TP receptors) on vascular smooth muscle. The purpose of the present study was to identify this EDCF by measuring changes in isometric tension and the release of various prostaglandins by acetylcholine. 2 In isolated aortic rings of SHR, U 46619, prostaglandin (PG) H 2, PGF 2α, PGE 2, PGD 2, prostacyclin (PGI 2) and 8-isoprostane, all activate TP receptors of the vascular smooth muscle to produce a contraction (U 46619≫8-isoprostane=PGF 2α=PGH 2>PGE 2=PGD 2> PGI 2). The contractions produced by PGH 2 and PGI 2 were fast and transient, mimicking endothelium-dependent contractions. PGI 2 did not relax isolated aortic rings of WKY and SHR. 3 Acetylcholine evoked the endothelium-dependent release of thromboxane A 2, PGF 2α, PGE 2, PGI 2 and most likely PGH 2 (PGI 2≫PGF 2α≥PGE 2>TXA 2>8-isoprostane, PGD 2). Dazoxiben abolished the production of thromboxane A 2, but did not influence the endothelium-dependent contractions to acetylcholine. 4 The release of PGI 2 was significantly larger in the aorta of SHR than in WKY, and the former was more sensitive to the contractile effect of PGI 2 than the latter. The inhibition of PGI-synthase was associated with an increase in PGH 2 spillover and the enhancement of acetylcholine-induced endothelium-dependent contractions. 5 Thus, in the aorta of SHR and aging WKY, the endothelium-dependent contractions elicited by acetylcholine most likely involve the release of PGI 2 with a concomitant contribution of PGH 2. © 2005 Nature Publishing Group All rights reserved.en_HK
dc.format.extent388 bytes-
dc.format.mimetypetext/html-
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.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectEndoperoxideen_HK
dc.subjectEndothelium-dependent contractionsen_HK
dc.subjectProstacyclinen_HK
dc.subjectProstaglandinsen_HK
dc.subjectSpontaneously hypertensive raten_HK
dc.subjectTP receptorsen_HK
dc.titleAcetylcholine-induced endothelium-dependent contractions in the SHR aorta: The Janus face of prostacyclinen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-1188&volume=146&issue=6&spage=834&epage=845&date=2005&atitle=Acetylcholine-induced+endothelium-dependent+contractions+in+the+SHR+aorta:+the+Janus+face+of+prostacyclinen_HK
dc.identifier.emailVanhoutte, PM: vanhoutt@hku.hken_HK
dc.identifier.authorityVanhoutte, PM=rp00238en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1038/sj.bjp.0706390en_HK
dc.identifier.pmid16158068-
dc.identifier.pmcidPMC1751221en_HK
dc.identifier.scopuseid_2-s2.0-27744564624en_HK
dc.identifier.hkuros119214-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27744564624&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume146en_HK
dc.identifier.issue6en_HK
dc.identifier.spage834en_HK
dc.identifier.epage845en_HK
dc.identifier.isiWOS:000233346200008-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridGluais, P=6602456462en_HK
dc.identifier.scopusauthoridLonchampt, M=7003363063en_HK
dc.identifier.scopusauthoridMorrow, JD=7202118461en_HK
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_HK
dc.identifier.scopusauthoridFeletou, M=7006461826en_HK

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