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Article: Ammonium ions cause relaxation of isolated canine arteries

TitleAmmonium ions cause relaxation of isolated canine arteries
Authors
Issue Date1989
PublisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.org
Citation
Journal Of Pharmacology And Experimental Therapeutics, 1989, v. 251 n. 1, p. 82-89 How to Cite?
AbstractExperiments were designed to determine the mechanism of action underlying relaxation of vascular smooth muscle induced by ammonium ions. In particular, the possibility that these ions might be an endothelium-derived relaxing factor was examined. Rings of large canine femoral, mesenteric and coronary arteries and of small arteries from the gracilis muscle were suspended in organ chambers for the recording of isometric force. Membrane potential was recorded with intracellular microelectrodes in smooth muscle cells from the mesenteric artery. Ammonium ions induced relaxations which were independent of the presence of the endothelium. The relaxations were not prevented by adrenergic, serotonergic, muscarinic and histaminic blockers, by scavengers of oxygen-derived radicals or by inhibitors of soluble guanylate cyclase. The relaxations were prevented by a decrease in extracellular calcium concentration and by inhibition of the Na+/K+ pump. The results are compatible with the hypothesis that the relaxation induced by ammonium ions is related to changes in intracellular pH and, at high concentration of these ions, possibly to activation of the Na+/K+ pump. Ammonium ions are neither the endothelium-derived relaxing factor which activates guanylate cyclase nor the factor that induces endothelium-derived hyperpolarization. Inasmuch as relatively low concentrations of the ion induce relaxation of small arteries of skeletal muscle, they could contribute to exercise hyperemia.
Persistent Identifierhttp://hdl.handle.net/10722/170944
ISSN
2015 Impact Factor: 3.76
2015 SCImago Journal Rankings: 1.847
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorFeletou, Men_US
dc.contributor.authorHarker, CTen_US
dc.contributor.authorKomori, Ken_US
dc.contributor.authorShepherd, JTen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:11:33Z-
dc.date.available2012-10-30T06:11:33Z-
dc.date.issued1989en_US
dc.identifier.citationJournal Of Pharmacology And Experimental Therapeutics, 1989, v. 251 n. 1, p. 82-89en_US
dc.identifier.issn0022-3565en_US
dc.identifier.urihttp://hdl.handle.net/10722/170944-
dc.description.abstractExperiments were designed to determine the mechanism of action underlying relaxation of vascular smooth muscle induced by ammonium ions. In particular, the possibility that these ions might be an endothelium-derived relaxing factor was examined. Rings of large canine femoral, mesenteric and coronary arteries and of small arteries from the gracilis muscle were suspended in organ chambers for the recording of isometric force. Membrane potential was recorded with intracellular microelectrodes in smooth muscle cells from the mesenteric artery. Ammonium ions induced relaxations which were independent of the presence of the endothelium. The relaxations were not prevented by adrenergic, serotonergic, muscarinic and histaminic blockers, by scavengers of oxygen-derived radicals or by inhibitors of soluble guanylate cyclase. The relaxations were prevented by a decrease in extracellular calcium concentration and by inhibition of the Na+/K+ pump. The results are compatible with the hypothesis that the relaxation induced by ammonium ions is related to changes in intracellular pH and, at high concentration of these ions, possibly to activation of the Na+/K+ pump. Ammonium ions are neither the endothelium-derived relaxing factor which activates guanylate cyclase nor the factor that induces endothelium-derived hyperpolarization. Inasmuch as relatively low concentrations of the ion induce relaxation of small arteries of skeletal muscle, they could contribute to exercise hyperemia.en_US
dc.languageengen_US
dc.publisherAmerican Society for Pharmacology and Experimental Therapeutics. The Journal's web site is located at http://jpet.aspetjournals.orgen_US
dc.relation.ispartofJournal of Pharmacology and Experimental Therapeuticsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Anatomy & Histology - Drug Effectsen_US
dc.subject.meshDogsen_US
dc.subject.meshFree Radicalsen_US
dc.subject.meshGuanylate Cyclase - Metabolismen_US
dc.subject.meshIon Exchangeen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshQuaternary Ammonium Compounds - Pharmacologyen_US
dc.subject.meshVasodilation - Drug Effectsen_US
dc.titleAmmonium ions cause relaxation of isolated canine arteriesen_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.pmid2571725-
dc.identifier.scopuseid_2-s2.0-0024466601en_US
dc.identifier.volume251en_US
dc.identifier.issue1en_US
dc.identifier.spage82en_US
dc.identifier.epage89en_US
dc.identifier.isiWOS:A1989AU47900012-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridFeletou, M=7006461826en_US
dc.identifier.scopusauthoridHarker, CT=7003742599en_US
dc.identifier.scopusauthoridKomori, K=8977740100en_US
dc.identifier.scopusauthoridShepherd, JT=7401742522en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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