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Article: Further investigation of endothelium-derived hyperpolarizing factor (EDHF) in rat hepatic artery: Studies using 1-EBIO and ouabain

TitleFurther investigation of endothelium-derived hyperpolarizing factor (EDHF) in rat hepatic artery: Studies using 1-EBIO and ouabain
Authors
Issue Date1999
PublisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1
Citation
British Journal Of Pharmacology, 1999, v. 128 n. 5, p. 1064-1070 How to Cite?
Abstract1. The characteristics of endothelium-dependent hyperpolarization in rat hepatic artery have been further investigated in the presence of inhibitors of cyclo-oxygenase and nitric oxide synthase. 2. Using sharp micro-electrodes, the smooth muscle hyperpolarization induced by acetylcholine, KCl or 1-ethyl-2-benzimidazolinone (1-EBIO) in intact hepatic arteries was abolished by 30 μM barium plus 500 nM ouabain. 3. In vessels without endothelium, the smooth muscle hyperpolarization induced by KCl was not reduced by 30 μM barium alone. However, in the presence of barium the effects of KCl were partially inhibited by 100 nM ouabain and essentially abolished by 500 nM ouabain. 4. Using sharp micro-electrodes, the hyperpolarization of both the smooth muscle and the endothelium induced by 1-EBIO or by acetylcholine was unaffected by 100 nM iberiotoxin. However, in the presence of 100 nM charybdotoxin, the effects of 1-EBIO were abolished whereas those of acetylcholine were only partially reduced. The hyperpolarization induced by levcromakalim was unaffected by either charybdotoxin or iberiotoxin. 5. Under whole-cell patch-clamp recording conditions, 1-EBIO induced a voltage-insensitive, charybdotoxin-sensitive K+ current in cultured endothelial cells but was without effect on K+ currents in smooth muscle cells isolated from hepatic arteries. 6. It is concluded that the endothelium-dependent hyperpolarization of smooth muscle induced by either acetylcholine or by 1-EBIO in rat hepatic artery is initially associated with the opening of endothelial calcium-sensitive K+-channels insensitive to iberiotoxin. The resulting accumulation of K+ in the myoendothelial space activates an isoform of Na+/K+-ATPase which is sensitive to low concentrations of ouabain.
Persistent Identifierhttp://hdl.handle.net/10722/171218
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
References

 

DC FieldValueLanguage
dc.contributor.authorEdwards, Gen_US
dc.contributor.authorGardener, MJen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorBrady, Gen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorWeston, AHen_US
dc.date.accessioned2012-10-30T06:12:46Z-
dc.date.available2012-10-30T06:12:46Z-
dc.date.issued1999en_US
dc.identifier.citationBritish Journal Of Pharmacology, 1999, v. 128 n. 5, p. 1064-1070en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171218-
dc.description.abstract1. The characteristics of endothelium-dependent hyperpolarization in rat hepatic artery have been further investigated in the presence of inhibitors of cyclo-oxygenase and nitric oxide synthase. 2. Using sharp micro-electrodes, the smooth muscle hyperpolarization induced by acetylcholine, KCl or 1-ethyl-2-benzimidazolinone (1-EBIO) in intact hepatic arteries was abolished by 30 μM barium plus 500 nM ouabain. 3. In vessels without endothelium, the smooth muscle hyperpolarization induced by KCl was not reduced by 30 μM barium alone. However, in the presence of barium the effects of KCl were partially inhibited by 100 nM ouabain and essentially abolished by 500 nM ouabain. 4. Using sharp micro-electrodes, the hyperpolarization of both the smooth muscle and the endothelium induced by 1-EBIO or by acetylcholine was unaffected by 100 nM iberiotoxin. However, in the presence of 100 nM charybdotoxin, the effects of 1-EBIO were abolished whereas those of acetylcholine were only partially reduced. The hyperpolarization induced by levcromakalim was unaffected by either charybdotoxin or iberiotoxin. 5. Under whole-cell patch-clamp recording conditions, 1-EBIO induced a voltage-insensitive, charybdotoxin-sensitive K+ current in cultured endothelial cells but was without effect on K+ currents in smooth muscle cells isolated from hepatic arteries. 6. It is concluded that the endothelium-dependent hyperpolarization of smooth muscle induced by either acetylcholine or by 1-EBIO in rat hepatic artery is initially associated with the opening of endothelial calcium-sensitive K+-channels insensitive to iberiotoxin. The resulting accumulation of K+ in the myoendothelial space activates an isoform of Na+/K+-ATPase which is sensitive to low concentrations of ouabain.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1en_US
dc.relation.ispartofBritish Journal of Pharmacologyen_US
dc.subject.meshAcetylcholine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBenzimidazoles - Pharmacologyen_US
dc.subject.meshBiological Factors - Pharmacologyen_US
dc.subject.meshCalcium Channel Agonists - Pharmacologyen_US
dc.subject.meshCromakalim - Pharmacologyen_US
dc.subject.meshElectrophysiologyen_US
dc.subject.meshEndothelium, Vascular - Cytology - Drug Effectsen_US
dc.subject.meshEnzyme Inhibitors - Pharmacologyen_US
dc.subject.meshHepatic Artery - Cytology - Drug Effectsen_US
dc.subject.meshMaleen_US
dc.subject.meshMicroelectrodesen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effectsen_US
dc.subject.meshOuabain - Pharmacologyen_US
dc.subject.meshPatch-Clamp Techniquesen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshPotassium Channels - Drug Effects - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshSodium-Potassium-Exchanging Atpase - Metabolismen_US
dc.subject.meshVasodilator Agents - Pharmacologyen_US
dc.titleFurther investigation of endothelium-derived hyperpolarizing factor (EDHF) in rat hepatic artery: Studies using 1-EBIO and ouabainen_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.doi10.1038/sj.bjp.0702916en_US
dc.identifier.pmid10556944-
dc.identifier.scopuseid_2-s2.0-0032712512en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032712512&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume128en_US
dc.identifier.issue5en_US
dc.identifier.spage1064en_US
dc.identifier.epage1070en_US
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US
dc.identifier.scopusauthoridGardener, MJ=6603795865en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridBrady, G=7005431765en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US

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