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Article: Relaxation of canine coronary artery to electrical stimulation: Limited role of free radicals

TitleRelaxation of canine coronary artery to electrical stimulation: Limited role of free radicals
Authors
Issue Date1987
PublisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/
Citation
American Journal Of Physiology - Heart And Circulatory Physiology, 1987, v. 253 n. 4, p. 22/4 How to Cite?
AbstractElectrical stimulation induces tetrodotoxin-insensitive relaxation of the canine coronary artery. The present study was designed to verify whether this relaxation involves the production of oxygen-derived free radicals. Isolated rings of canine coronary arteries were suspended from isometric tension recording in organ chambers filled with Krebs-Ringer bicarbonate solution. They were stimulated electrically (9 V, 3 Hz, 2 ms for 2 min) by means of two platinum electrodes during contractions evoked by various vasoactive agonists. Under control conditions, electrical stimulation caused rapid, reversible relaxations. Superoxide dismutase in association with catalase or mannitol, sodium ascorbate, dimethyl sulfoxide, and glutathione did not inhibit the relaxation caused by stimulation applied for only 2 min; neither did the removal of chloride ions from the salt solution nor the association of Cl-free solution in the presence of mannitol, superoxide dismutase, and catalase. Prolonging the electrical stimulation (9 V, 3 Hz, 2 ms) for up to 20 min produced a secondary relaxation. This second phase was inhibited by sodium ascorbate. These experiments indicate that the rapid relaxation induced by short-lasting electrical stimulation is probably not due to the generation of oxygen-derived free radicals. However, prolonged stimulation causes the production of such radicals, which then evoked irreversible inhibition of the vascular smooth muscle of the canine coronary artery.
Persistent Identifierhttp://hdl.handle.net/10722/170863
ISSN
1998 Impact Factor: 3.077
2004 SCImago Journal Rankings: 1.102
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFeletou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:10Z-
dc.date.available2012-10-30T06:11:10Z-
dc.date.issued1987en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1987, v. 253 n. 4, p. 22/4en_US
dc.identifier.issn0002-9513en_US
dc.identifier.urihttp://hdl.handle.net/10722/170863-
dc.description.abstractElectrical stimulation induces tetrodotoxin-insensitive relaxation of the canine coronary artery. The present study was designed to verify whether this relaxation involves the production of oxygen-derived free radicals. Isolated rings of canine coronary arteries were suspended from isometric tension recording in organ chambers filled with Krebs-Ringer bicarbonate solution. They were stimulated electrically (9 V, 3 Hz, 2 ms for 2 min) by means of two platinum electrodes during contractions evoked by various vasoactive agonists. Under control conditions, electrical stimulation caused rapid, reversible relaxations. Superoxide dismutase in association with catalase or mannitol, sodium ascorbate, dimethyl sulfoxide, and glutathione did not inhibit the relaxation caused by stimulation applied for only 2 min; neither did the removal of chloride ions from the salt solution nor the association of Cl-free solution in the presence of mannitol, superoxide dismutase, and catalase. Prolonging the electrical stimulation (9 V, 3 Hz, 2 ms) for up to 20 min produced a secondary relaxation. This second phase was inhibited by sodium ascorbate. These experiments indicate that the rapid relaxation induced by short-lasting electrical stimulation is probably not due to the generation of oxygen-derived free radicals. However, prolonged stimulation causes the production of such radicals, which then evoked irreversible inhibition of the vascular smooth muscle of the canine coronary artery.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://ajpcon.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAscorbic Acid - Pharmacologyen_US
dc.subject.meshCatalase - Metabolismen_US
dc.subject.meshCoronary Vessels - Physiologyen_US
dc.subject.meshDimethyl Sulfoxide - Pharmacologyen_US
dc.subject.meshDinoprosten_US
dc.subject.meshDogsen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFree Radicalsen_US
dc.subject.meshGlutathione - Pharmacologyen_US
dc.subject.meshHistamine - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMannitol - Pharmacologyen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPotassium Chloride - Pharmacologyen_US
dc.subject.meshProstaglandins F - Pharmacologyen_US
dc.subject.meshSuperoxide Dismutase - Metabolismen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.subject.meshVasodilationen_US
dc.titleRelaxation of canine coronary artery to electrical stimulation: Limited role of free radicalsen_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.pmid3116861-
dc.identifier.scopuseid_2-s2.0-0023622945en_US
dc.identifier.volume253en_US
dc.identifier.issue4en_US
dc.identifier.spage22/4en_US
dc.identifier.isiWOS:A1987K518300023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFeletou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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