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Article: Endothelium-dependent contractions to arachidonic acid are mediated by products of cyclooxygenase

TitleEndothelium-dependent contractions to arachidonic acid are mediated by products of cyclooxygenase
Authors
Issue Date1985
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, 1985, v. 17 n. 4, p. H432-H437 How to Cite?
AbstractArachidonic acid produces endothelium-dependent relaxation in canine arteries and endothelium-dependent contraction in veins. In canine femoral arteries, the relaxation is prevented by inhibitors of cyclooxygenase. To determine the role of cyclooxygenase in the contraction evoked by arachidonic acid in the veins, rings of canine femoral and intrapulmonary veins, with and without endothelium, were suspended in organ chambers and set at their optimum length for isometric tension measurements. In rings of femoral and pulmonary vein contracted with norepinephrine, arachidonic acid produced a concentration-dependent increase in tension that was eliminated by removal of the endothelium or by treatment with the inhibitors of cyclooxygenase (indomethacin, meclofenamate, or acetylsalicyclic acid). The contractions were not prevented by inhibitors of thromboxane synthetase or prostacyclin synthetase or lipoxygenase. Pulmonary and femoral veins with or without endothelium relaxed to low, but contracted to high concentrations of prostacyclin and prostaglandin E2. Prostaglandin F2(α) caused endothelium-independent contractions in both blood vessels. The present study suggests that the endothelium-dependent contractions to arachidonic acid observed in canine veins are mediated by prostanoids other than tromboxane and prostacyclin.
Persistent Identifierhttp://hdl.handle.net/10722/170765
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823

 

DC FieldValueLanguage
dc.contributor.authorMiller, VMen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:45Z-
dc.date.available2012-10-30T06:10:45Z-
dc.date.issued1985en_US
dc.identifier.citationAmerican Journal Of Physiology - Heart And Circulatory Physiology, 1985, v. 17 n. 4, p. H432-H437en_US
dc.identifier.issn0363-6135en_US
dc.identifier.urihttp://hdl.handle.net/10722/170765-
dc.description.abstractArachidonic acid produces endothelium-dependent relaxation in canine arteries and endothelium-dependent contraction in veins. In canine femoral arteries, the relaxation is prevented by inhibitors of cyclooxygenase. To determine the role of cyclooxygenase in the contraction evoked by arachidonic acid in the veins, rings of canine femoral and intrapulmonary veins, with and without endothelium, were suspended in organ chambers and set at their optimum length for isometric tension measurements. In rings of femoral and pulmonary vein contracted with norepinephrine, arachidonic acid produced a concentration-dependent increase in tension that was eliminated by removal of the endothelium or by treatment with the inhibitors of cyclooxygenase (indomethacin, meclofenamate, or acetylsalicyclic acid). The contractions were not prevented by inhibitors of thromboxane synthetase or prostacyclin synthetase or lipoxygenase. Pulmonary and femoral veins with or without endothelium relaxed to low, but contracted to high concentrations of prostacyclin and prostaglandin E2. Prostaglandin F2(α) caused endothelium-independent contractions in both blood vessels. The present study suggests that the endothelium-dependent contractions to arachidonic acid observed in canine veins are mediated by prostanoids other than tromboxane and prostacyclin.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.titleEndothelium-dependent contractions to arachidonic acid are mediated by products of cyclooxygenaseen_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.scopuseid_2-s2.0-0021824270en_US
dc.identifier.volume17en_US
dc.identifier.issue4en_US
dc.identifier.spageH432en_US
dc.identifier.epageH437en_US
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridMiller, VM=7201476816en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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