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Conference Paper: Thromboxane A2 receptor antagonists inhibit endothelium-dependent contractions

TitleThromboxane A2 receptor antagonists inhibit endothelium-dependent contractions
Authors
Issue Date1990
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1990, v. 15 n. 6 II, p. 699-703 How to Cite?
AbstractEndothelium-dependent contractions to acetylcholine and endothelium-independent contractions to oxygen-derived free radicals in the aorta of the spontaneously hypertensive rat (SHR) are mediated by an unidentified product of the cyclooxygenase pathway of arachidonic acid metabolism. To determine the role of thromboxane A2 (TXA2) or prostaglandin H2 (PGH2) in these contractions, rings of the thoracic aorta of SHR were suspended in organ chambers for measurement of isometric force. Acetylcholine caused endothelium-dependent contractions in quiescent rings from SHR aortas. Oxygen-derived free radicals generated with xanthine plus xanthine oxidase caused contractions in rings without endothelium. Dazoxiben (thromboxane synthetase inhibitor) did not affect contractions evoked by acetylcholine. AH 23,848, SQ 29,548, or R 68,070 (TXA2/PGH2 receptor antagonists) inhibited contractions to U 46,619 (a TXA2/PGH2 receptor antagonist), acetylcholine, and oxygen-derived free radicals. Acetylcholine stimulated the release of prostacyclin from Wistar-Kyoto (WKY) rat and SHR aortas but not the release of other prostaglandins (PGE2, PGF(2α), TXA2). Oxygen-derived free radicals did not stimulate the release of prostaglandins from either SHR or WKY rat aortas. These results demonstrate that stimulation of TXA2/PGH2 receptors probably by PGH2 might be involved in endothelium-dependent contractions. Oxygen-derived free radicals, which might be an endothelium-derived contracting factor or factors, ultimately cause contraction by stimulation of TXA2/PGH2 receptors.
Persistent Identifierhttp://hdl.handle.net/10722/173481
ISSN
2015 Impact Factor: 6.294
2015 SCImago Journal Rankings: 3.702
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAuchSchwelk, Wen_US
dc.contributor.authorKatusic, ZSen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:32:16Z-
dc.date.available2012-10-30T06:32:16Z-
dc.date.issued1990en_US
dc.identifier.citationHypertension, 1990, v. 15 n. 6 II, p. 699-703en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/173481-
dc.description.abstractEndothelium-dependent contractions to acetylcholine and endothelium-independent contractions to oxygen-derived free radicals in the aorta of the spontaneously hypertensive rat (SHR) are mediated by an unidentified product of the cyclooxygenase pathway of arachidonic acid metabolism. To determine the role of thromboxane A2 (TXA2) or prostaglandin H2 (PGH2) in these contractions, rings of the thoracic aorta of SHR were suspended in organ chambers for measurement of isometric force. Acetylcholine caused endothelium-dependent contractions in quiescent rings from SHR aortas. Oxygen-derived free radicals generated with xanthine plus xanthine oxidase caused contractions in rings without endothelium. Dazoxiben (thromboxane synthetase inhibitor) did not affect contractions evoked by acetylcholine. AH 23,848, SQ 29,548, or R 68,070 (TXA2/PGH2 receptor antagonists) inhibited contractions to U 46,619 (a TXA2/PGH2 receptor antagonist), acetylcholine, and oxygen-derived free radicals. Acetylcholine stimulated the release of prostacyclin from Wistar-Kyoto (WKY) rat and SHR aortas but not the release of other prostaglandins (PGE2, PGF(2α), TXA2). Oxygen-derived free radicals did not stimulate the release of prostaglandins from either SHR or WKY rat aortas. These results demonstrate that stimulation of TXA2/PGH2 receptors probably by PGH2 might be involved in endothelium-dependent contractions. Oxygen-derived free radicals, which might be an endothelium-derived contracting factor or factors, ultimately cause contraction by stimulation of TXA2/PGH2 receptors.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_US
dc.relation.ispartofHypertensionen_US
dc.subject.mesh15-Hydroxy-11 Alpha,9 Alpha-(Epoxymethano)Prosta-5,13-Dienoic Aciden_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFree Radicalsen_US
dc.subject.meshMaleen_US
dc.subject.meshOxygen - Metabolismen_US
dc.subject.meshProstaglandin Endoperoxides, Synthetic - Pharmacologyen_US
dc.subject.meshProstaglandins - Biosynthesisen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshReceptors, Prostaglandin - Physiologyen_US
dc.subject.meshReceptors, Thromboxaneen_US
dc.subject.meshThromboxanes - Metabolismen_US
dc.subject.meshVasoconstriction - Physiologyen_US
dc.titleThromboxane A2 receptor antagonists inhibit endothelium-dependent contractionsen_US
dc.typeConference_Paperen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1161/01.HYP.15.6.699-
dc.identifier.pmid2141003-
dc.identifier.scopuseid_2-s2.0-0025440112en_US
dc.identifier.volume15en_US
dc.identifier.issue6 IIen_US
dc.identifier.spage699en_US
dc.identifier.epage703en_US
dc.identifier.isiWOS:A1990DH51800007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridAuchSchwelk, W=7003395589en_US
dc.identifier.scopusauthoridKatusic, ZS=7006971465en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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