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Article: Contractions to oxygen-derived free radicals are augmented in aorta of the spontaneously hypertensive rat

TitleContractions to oxygen-derived free radicals are augmented in aorta of the spontaneously hypertensive rat
Authors
Issue Date1989
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1989, v. 13 n. 6 II, p. 859-864 How to Cite?
AbstractTo determine if oxygen-derived free radicals are mediators of endothelium-dependent contractions to acetylcholine in the aorta of spontaneously hypertensive rats (SHR), the mechanism of contraction to xanthine plus xanthine oxidase was studied. Rings, with and without endothelium, or thoracic aorta from normotensive Wistar-Kyoto (WKY) rats and SHR were suspended in organ chambers for isometric tension recording. Oxygen-derived free radicals caused concentration-dependent contractions; these contractions were twice as large in the aortas of SHR than in WKY rats. Deferoxamine reversed the response to xanthine oxidase to a small relaxation. Either allopurinol, superoxide dismutase, or catalase, or the combination of superoxide dismutase plus catalase reduced the contractions. Diltiazem inhibited the response to xanthine oxidase; in contrast, phentolamine plus propranolol did not affect it. Indomethacin and meclofenamate, but not tranylcypromine or dazoxiben blocked the contractions. Endothelium-dependent contractions to acetylcholine in aortas from the SHR were not affected by deferoxamine or superoxide dismutase plus catalase. These data suggest that hydroxyl radicals cause contractions in the rat aorta, which are dependent on extracellular calcium and mediated by activation of the cyclooxygenase in the vascular smooth muscle. The augmented contractions in the hypertensive strain are due to an increased reactivity of the smooth muscle to oxygen-derived free radicals. However, the lack of the effect of the scavengers on endothelium-dependent contractions to acetylcholine suggests that the endothelium-derived contracting factor is chemically different from oxygen-derived free radicals.
Persistent Identifierhttp://hdl.handle.net/10722/170930
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.accessioned2012-10-30T06:11:28Z-
dc.date.available2012-10-30T06:11:28Z-
dc.date.issued1989en_US
dc.identifier.citationHypertension, 1989, v. 13 n. 6 II, p. 859-864en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170930-
dc.description.abstractTo determine if oxygen-derived free radicals are mediators of endothelium-dependent contractions to acetylcholine in the aorta of spontaneously hypertensive rats (SHR), the mechanism of contraction to xanthine plus xanthine oxidase was studied. Rings, with and without endothelium, or thoracic aorta from normotensive Wistar-Kyoto (WKY) rats and SHR were suspended in organ chambers for isometric tension recording. Oxygen-derived free radicals caused concentration-dependent contractions; these contractions were twice as large in the aortas of SHR than in WKY rats. Deferoxamine reversed the response to xanthine oxidase to a small relaxation. Either allopurinol, superoxide dismutase, or catalase, or the combination of superoxide dismutase plus catalase reduced the contractions. Diltiazem inhibited the response to xanthine oxidase; in contrast, phentolamine plus propranolol did not affect it. Indomethacin and meclofenamate, but not tranylcypromine or dazoxiben blocked the contractions. Endothelium-dependent contractions to acetylcholine in aortas from the SHR were not affected by deferoxamine or superoxide dismutase plus catalase. These data suggest that hydroxyl radicals cause contractions in the rat aorta, which are dependent on extracellular calcium and mediated by activation of the cyclooxygenase in the vascular smooth muscle. The augmented contractions in the hypertensive strain are due to an increased reactivity of the smooth muscle to oxygen-derived free radicals. However, the lack of the effect of the scavengers on endothelium-dependent contractions to acetylcholine suggests that the endothelium-derived contracting factor is chemically different from oxygen-derived free radicals.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.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Pharmacologyen_US
dc.subject.meshAllopurinol - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta - Drug Effects - Metabolismen_US
dc.subject.meshArachidonic Aciden_US
dc.subject.meshArachidonic Acids - Metabolismen_US
dc.subject.meshDiltiazem - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Physiologyen_US
dc.subject.meshFree Radicalsen_US
dc.subject.meshHypertension - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshOxygen - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshXanthine Oxidase - Antagonists & Inhibitors - Pharmacologyen_US
dc.titleContractions to oxygen-derived free radicals are augmented in aorta of the spontaneously hypertensive raten_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.doi10.1161/01.HYP.13.6.859-
dc.identifier.pmid2567706-
dc.identifier.scopuseid_2-s2.0-0024402398en_US
dc.identifier.volume13en_US
dc.identifier.issue6 IIen_US
dc.identifier.spage859en_US
dc.identifier.epage864en_US
dc.identifier.isiWOS:A1989AA58200031-
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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