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Article: Endothelium-dependent contractions are associated with both augmented expression of prostaglandin H synthase-1 and hypersensitivity to prostaglandin H 2 in the SHR aorta

TitleEndothelium-dependent contractions are associated with both augmented expression of prostaglandin H synthase-1 and hypersensitivity to prostaglandin H 2 in the SHR aorta
Authors
Issue Date1995
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1995, v. 76 n. 6, p. 1003-1010 How to Cite?
AbstractProstaglandin H 2 (PGH 2 [endoperoxide]) is an immediate product of prostaglandin H (PGH) synthase activity (cyclooxygenase) and a likely candidate to mediate endothelium-dependent contractions evoked by acetylcholine in the aorta of the spontaneously hypertensive rat (SHR). Experiments were designed to investigate whether or not endothelium-dependent contractions were associated with an increased expression of PGH synthase, an augmented acetylcholine-induced release of PGH 2, and/or a hypersensitivity of the smooth muscle to endoperoxides in SHR aorta compared with normotensive Wistar-Kyoto (WKY) aorta. In SHR aorta, endothelium-dependent contractions to acetylcholine were abolished by tenidap (10 -8 mol/L), a preferential PGH synthase-1 inhibitor, but slightly impaired by NS-398 (10 -6 mol/L), a preferential PGH synthase-2 inhibitor. PGH synthase-1 expression, which was evaluated by both reverse transcriptase-polymerase chain reaction and Western blotting, was about twofold greater in preparations with endothelium from SHR than from WKY rats. There was no difference in PGH synthase-1 expression between preparations with and those without endothelium in both strains. In SHR but not WKY aortas, acetylcholine (10 -5 mol/L, 5 minutes) caused a significant endothelium-dependent release of PGH 2, as measured by gas chromatography/mass spectrometry. PGH 2 evoked more potent contractions in rings without endothelium from SHR than from WKY rats, whereas the thromboxane analogue U46619 and prostaglandin F(2α) caused a comparable response in both preparations. These results show that endothelium-dependent contractions to acetylcholine in SHR aorta are associated with a greater expression of PGH synthase-1, a significant release of PGH 2, and a hypersensitivity of the smooth muscle to the endoperoxide.
Persistent Identifierhttp://hdl.handle.net/10722/171167
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorGe, Ten_US
dc.contributor.authorHughes, Hen_US
dc.contributor.authorJunquero, DCen_US
dc.contributor.authorWu, KKen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBoulanger, CMen_US
dc.date.accessioned2012-10-30T06:12:30Z-
dc.date.available2012-10-30T06:12:30Z-
dc.date.issued1995en_US
dc.identifier.citationCirculation Research, 1995, v. 76 n. 6, p. 1003-1010en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/171167-
dc.description.abstractProstaglandin H 2 (PGH 2 [endoperoxide]) is an immediate product of prostaglandin H (PGH) synthase activity (cyclooxygenase) and a likely candidate to mediate endothelium-dependent contractions evoked by acetylcholine in the aorta of the spontaneously hypertensive rat (SHR). Experiments were designed to investigate whether or not endothelium-dependent contractions were associated with an increased expression of PGH synthase, an augmented acetylcholine-induced release of PGH 2, and/or a hypersensitivity of the smooth muscle to endoperoxides in SHR aorta compared with normotensive Wistar-Kyoto (WKY) aorta. In SHR aorta, endothelium-dependent contractions to acetylcholine were abolished by tenidap (10 -8 mol/L), a preferential PGH synthase-1 inhibitor, but slightly impaired by NS-398 (10 -6 mol/L), a preferential PGH synthase-2 inhibitor. PGH synthase-1 expression, which was evaluated by both reverse transcriptase-polymerase chain reaction and Western blotting, was about twofold greater in preparations with endothelium from SHR than from WKY rats. There was no difference in PGH synthase-1 expression between preparations with and those without endothelium in both strains. In SHR but not WKY aortas, acetylcholine (10 -5 mol/L, 5 minutes) caused a significant endothelium-dependent release of PGH 2, as measured by gas chromatography/mass spectrometry. PGH 2 evoked more potent contractions in rings without endothelium from SHR than from WKY rats, whereas the thromboxane analogue U46619 and prostaglandin F(2α) caused a comparable response in both preparations. These results show that endothelium-dependent contractions to acetylcholine in SHR aorta are associated with a greater expression of PGH synthase-1, a significant release of PGH 2, and a hypersensitivity of the smooth muscle to the endoperoxide.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Drug Effects - Immunology - Physiologyen_US
dc.subject.meshAutoradiographyen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshGene Amplificationen_US
dc.subject.meshHypersensitivityen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contractionen_US
dc.subject.meshMuscle, Smooth, Vascular - Immunology - Physiologyen_US
dc.subject.meshPolymerase Chain Reactionen_US
dc.subject.meshProstaglandin H2en_US
dc.subject.meshProstaglandin-Endoperoxide Synthases - Analysis - Geneticsen_US
dc.subject.meshProstaglandins H - Analysis - Immunologyen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshTranscription, Geneticen_US
dc.titleEndothelium-dependent contractions are associated with both augmented expression of prostaglandin H synthase-1 and hypersensitivity to prostaglandin H 2 in the SHR aortaen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid7758154-
dc.identifier.scopuseid_2-s2.0-0029079634en_US
dc.identifier.volume76en_US
dc.identifier.issue6en_US
dc.identifier.spage1003en_US
dc.identifier.epage1010en_US
dc.identifier.isiWOS:A1995QZ49700011-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridGe, T=7003328740en_US
dc.identifier.scopusauthoridHughes, H=7202659303en_US
dc.identifier.scopusauthoridJunquero, DC=26643025500en_US
dc.identifier.scopusauthoridWu, KK=7404512552en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBoulanger, CM=7006599024en_US

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