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Article: Oxygen-derived free radicals, endothelium, and responsiveness of vascular smooth muscle

TitleOxygen-derived free radicals, endothelium, and responsiveness of vascular smooth muscle
Authors
Issue Date1986
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1986, v. 250 n. 5, p. 19/5 How to Cite?
AbstractExperiments were designed to determine the role of oxygen-derived free radicals in modulating contractions of vascular smooth muscle and endothelium-mediated relaxations to acetylcholine. The effects of generating or scavenging these radicals were studied in rings of canine coronary arteries suspended for isometric tension recording. Xanthine oxidase plus xanthine caused relaxations, which were greater in rings with endothelium than in rings without endothelium; the relaxations were not affected by superoxide dismutase or mannitol, but could be prevented by catalase. Xanthine oxidase plus xanthine depressed endothelium-mediated relaxations to acetylcholine; this effect was prevented by superoxide dismutase, but was not affected by catalase or mannitol. Exogenous hydrogen peroxide induced catalase-sensitive relaxations, which were depressed by the removal of the endothelium. Superoxide dismutase evoked catalase-sensitive relaxations only in rings with endothelium. Endothelium-mediated relaxations to acetylcholine were slightly depressed by superoxide dismutase or catalase alone; the combination of the two enzymes or mannitol caused a major shift to the right of the concentration-response curve to acetylcholine. In rings without endothelium, relaxations caused by sodium nitroprusside were not affected by the scavengers (alone or in combination) but were augmented by xanthine oxidase plus xanthine. These data suggest that 1) the endothelium-derived relaxing factor released by acetylcholine is not likely to be an oxygen-derived free radical; 2) hydrogen peroxide has a direct inhibitory action on coronary arterial smooth muscle and triggers endothelium-dependent relaxations; and 3) superoxide anions depress and hydroxyl radicals facilitate endothelium-dependent relaxations caused by activation of muscarinic receptors.
Persistent Identifierhttp://hdl.handle.net/10722/170807
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorRubanyi, GMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:56Z-
dc.date.available2012-10-30T06:10:56Z-
dc.date.issued1986en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1986, v. 250 n. 5, p. 19/5en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/170807-
dc.description.abstractExperiments were designed to determine the role of oxygen-derived free radicals in modulating contractions of vascular smooth muscle and endothelium-mediated relaxations to acetylcholine. The effects of generating or scavenging these radicals were studied in rings of canine coronary arteries suspended for isometric tension recording. Xanthine oxidase plus xanthine caused relaxations, which were greater in rings with endothelium than in rings without endothelium; the relaxations were not affected by superoxide dismutase or mannitol, but could be prevented by catalase. Xanthine oxidase plus xanthine depressed endothelium-mediated relaxations to acetylcholine; this effect was prevented by superoxide dismutase, but was not affected by catalase or mannitol. Exogenous hydrogen peroxide induced catalase-sensitive relaxations, which were depressed by the removal of the endothelium. Superoxide dismutase evoked catalase-sensitive relaxations only in rings with endothelium. Endothelium-mediated relaxations to acetylcholine were slightly depressed by superoxide dismutase or catalase alone; the combination of the two enzymes or mannitol caused a major shift to the right of the concentration-response curve to acetylcholine. In rings without endothelium, relaxations caused by sodium nitroprusside were not affected by the scavengers (alone or in combination) but were augmented by xanthine oxidase plus xanthine. These data suggest that 1) the endothelium-derived relaxing factor released by acetylcholine is not likely to be an oxygen-derived free radical; 2) hydrogen peroxide has a direct inhibitory action on coronary arterial smooth muscle and triggers endothelium-dependent relaxations; and 3) superoxide anions depress and hydroxyl radicals facilitate endothelium-dependent relaxations caused by activation of muscarinic receptors.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpheart.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCatalase - Pharmacologyen_US
dc.subject.meshDogsen_US
dc.subject.meshEndothelium - Drug Effects - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFree Radicalsen_US
dc.subject.meshHydrogen Peroxide - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMannitol - Pharmacologyen_US
dc.subject.meshMuscle Relaxation - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Drug Effects - Physiologyen_US
dc.subject.meshNitroprusside - Pharmacologyen_US
dc.subject.meshOxygen - Metabolismen_US
dc.subject.meshSuperoxide Dismutase - Pharmacologyen_US
dc.subject.meshXanthineen_US
dc.subject.meshXanthine Oxidase - Pharmacologyen_US
dc.subject.meshXanthines - Pharmacologyen_US
dc.titleOxygen-derived free radicals, endothelium, and responsiveness of vascular smooth muscleen_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.pmid3085520-
dc.identifier.scopuseid_2-s2.0-0022456638en_US
dc.identifier.volume250en_US
dc.identifier.issue5en_US
dc.identifier.spage19/5en_US
dc.identifier.isiWOS:A1986C334900017-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridRubanyi, GM=7005517991en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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