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Article: Nitric oxide inactivates endothelium-derived contracting factor in the rat aorta

TitleNitric oxide inactivates endothelium-derived contracting factor in the rat aorta
Authors
Issue Date1992
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1992, v. 19 n. 5, p. 442-445 How to Cite?
AbstractAcetylcholine evokes the simultaneous release of endothelium-derived relaxing and contracting factors in aortas from spontaneously hypertensive rats. Only relaxing factors are released in aortas from normotensive controls. Experiments were designed to determine whether inhibitors of endothelium-dependent relaxations modify endothelium-dependent contractions. Rings of thoracic aortas of normotensive and spontaneously hypertensive rats, with and without endothelium, were suspended in organ chambers for isometric tension recording. Oxyhemoglobin (a scavenger of endothelium-derived relaxing factor) and N(G)-monomethyl L-arginine (an inhibitor of nitric oxide formation) augmented the contractions to acetylcholine. Methylene blue (an inhibitor of soluble guanylate cyclase) and superoxide dismutase (a scavenger of superoxide anions) did not modify these contractions. The contractions in the presence of oxyhemoglobin or N(G)-monomethyl L-arginine, like those in untreated rings, were endothelium-dependent; they only occurred in aortas from spontaneously hypertensive rats and were abolished by indomethacin. The contractions to acetylcholine in the presence of oxyhemoglobin were not affected by superoxide dismutase or deferoxamine. These data suggest that endothelium-derived relaxing factor inhibits endothelium-dependent contractions to acetylcholine in the spontaneously hypertensive rat aorta, probably by chemical inactivation of the endothelium-derived contracting factor rather than by stimulation of guanylate cyclase or scavenging of oxygen-derived free radicals.
Persistent Identifierhttp://hdl.handle.net/10722/171069
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.accessioned2012-10-30T06:12:04Z-
dc.date.available2012-10-30T06:12:04Z-
dc.date.issued1992en_US
dc.identifier.citationHypertension, 1992, v. 19 n. 5, p. 442-445en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171069-
dc.description.abstractAcetylcholine evokes the simultaneous release of endothelium-derived relaxing and contracting factors in aortas from spontaneously hypertensive rats. Only relaxing factors are released in aortas from normotensive controls. Experiments were designed to determine whether inhibitors of endothelium-dependent relaxations modify endothelium-dependent contractions. Rings of thoracic aortas of normotensive and spontaneously hypertensive rats, with and without endothelium, were suspended in organ chambers for isometric tension recording. Oxyhemoglobin (a scavenger of endothelium-derived relaxing factor) and N(G)-monomethyl L-arginine (an inhibitor of nitric oxide formation) augmented the contractions to acetylcholine. Methylene blue (an inhibitor of soluble guanylate cyclase) and superoxide dismutase (a scavenger of superoxide anions) did not modify these contractions. The contractions in the presence of oxyhemoglobin or N(G)-monomethyl L-arginine, like those in untreated rings, were endothelium-dependent; they only occurred in aortas from spontaneously hypertensive rats and were abolished by indomethacin. The contractions to acetylcholine in the presence of oxyhemoglobin were not affected by superoxide dismutase or deferoxamine. These data suggest that endothelium-derived relaxing factor inhibits endothelium-dependent contractions to acetylcholine in the spontaneously hypertensive rat aorta, probably by chemical inactivation of the endothelium-derived contracting factor rather than by stimulation of guanylate cyclase or scavenging of 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 - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAorta, Thoracicen_US
dc.subject.meshArginine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Drug Effectsen_US
dc.subject.meshFree Radical Scavengersen_US
dc.subject.meshHypertension - Metabolism - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMethylene Blue - Pharmacologyen_US
dc.subject.meshNitric Oxide - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshOxygen - Metabolismen_US
dc.subject.meshOxyhemoglobins - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Inbred Shren_US
dc.subject.meshRats, Inbred Wkyen_US
dc.subject.meshSuperoxide Dismutase - Antagonists & Inhibitors - Metabolismen_US
dc.subject.meshOmega-N-Methylarginineen_US
dc.titleNitric oxide inactivates endothelium-derived contracting factor in the rat aortaen_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.19.5.442-
dc.identifier.pmid1568762-
dc.identifier.scopuseid_2-s2.0-0026717033en_US
dc.identifier.volume19en_US
dc.identifier.issue5en_US
dc.identifier.spage442en_US
dc.identifier.epage445en_US
dc.identifier.isiWOS:A1992HT01600007-
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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