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Article: Suppression of K +-induced hyperpolarization by phenylephrine in rat mesenteric artery: Relevance to studies of endothelium-derived hyperpolarizing factor

TitleSuppression of K +-induced hyperpolarization by phenylephrine in rat mesenteric artery: Relevance to studies of endothelium-derived hyperpolarizing factor
Authors
Issue Date2001
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, 2001, v. 134 n. 1, p. 1-5 How to Cite?
AbstractIn intact mesenteric arteries, increasing [K +] o by 5 mM hyperpolarized both endothelial and smooth muscle cells. Subsequent exposure to 10 μM phenylephrine depolarized both cell types which were then repolarized by a 5 mM increase in [K +] o. In endothelium-denuded vessels, increasing [K +] o by 5 mM hyperpolarized the smooth muscle but K + had no effect after depolarization by 10 μM phenylephrine. On subsequent exposure to iberiotoxin plus 4-aminopyridine, the repolarizing action of 5 mM K + was restored. In endothelium-intact vessels exposed to phenylephrine, pretreatment with a gap junction inhibitor (gap 27) reduced K +-mediated smooth muscle repolarization without affecting the endothelial cell response. It is concluded that phenylephrine-induced efflux of K + via smooth muscle K + channels produces a local increase in [K +] o which impairs repolarization to added K +. Thus, studies involving vessels precontracted with agonists which increase [K +] o maximize the role of gap junctions and minimize any contribution to the EDHF pathway from endothelium-derived K +.
Persistent Identifierhttp://hdl.handle.net/10722/171257
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRichards, GRen_US
dc.contributor.authorWeston, AHen_US
dc.contributor.authorBurnham, MPen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorEdwards, Gen_US
dc.date.accessioned2012-10-30T06:13:00Z-
dc.date.available2012-10-30T06:13:00Z-
dc.date.issued2001en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2001, v. 134 n. 1, p. 1-5en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171257-
dc.description.abstractIn intact mesenteric arteries, increasing [K +] o by 5 mM hyperpolarized both endothelial and smooth muscle cells. Subsequent exposure to 10 μM phenylephrine depolarized both cell types which were then repolarized by a 5 mM increase in [K +] o. In endothelium-denuded vessels, increasing [K +] o by 5 mM hyperpolarized the smooth muscle but K + had no effect after depolarization by 10 μM phenylephrine. On subsequent exposure to iberiotoxin plus 4-aminopyridine, the repolarizing action of 5 mM K + was restored. In endothelium-intact vessels exposed to phenylephrine, pretreatment with a gap junction inhibitor (gap 27) reduced K +-mediated smooth muscle repolarization without affecting the endothelial cell response. It is concluded that phenylephrine-induced efflux of K + via smooth muscle K + channels produces a local increase in [K +] o which impairs repolarization to added K +. Thus, studies involving vessels precontracted with agonists which increase [K +] o maximize the role of gap junctions and minimize any contribution to the EDHF pathway from endothelium-derived K +.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.mesh4-Aminopyridine - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshConnexins - Pharmacologyen_US
dc.subject.meshEndothelium, Vascular - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Potentials - Drug Effectsen_US
dc.subject.meshMesenteric Arteries - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshMuscle, Smooth, Vascular - Cytology - Drug Effects - Physiologyen_US
dc.subject.meshPeptides - Pharmacologyen_US
dc.subject.meshPhenylephrine - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshVasoconstrictor Agents - Pharmacologyen_US
dc.titleSuppression of K +-induced hyperpolarization by phenylephrine in rat mesenteric artery: Relevance to studies of endothelium-derived hyperpolarizing factoren_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.0704256-
dc.identifier.pmid11522590-
dc.identifier.scopuseid_2-s2.0-0034840209en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034840209&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume134en_US
dc.identifier.issue1en_US
dc.identifier.spage1en_US
dc.identifier.epage5en_US
dc.identifier.isiWOS:000170792200001-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridRichards, GR=7201583688en_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US
dc.identifier.scopusauthoridBurnham, MP=7004848578en_US
dc.identifier.scopusauthoridFélétou, M=7006461826en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridEdwards, G=7402317535en_US

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