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Article: K +-induced hyperpolarization in rat mesenteric artery: Identification, localization and role of Na +/K +-ATPases

TitleK +-induced hyperpolarization in rat mesenteric artery: Identification, localization and role of Na +/K +-ATPases
Authors
Keywords4-Aminopyridine
Edhf
Hyperpolarization
Iberiotoxin
Immuno-Histochemistry
Na +/K +-Atpase Isoforms
Ouabain
Phenylephrine
Potassium
Issue Date2002
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, 2002, v. 136 n. 6, p. 918-926 How to Cite?
Abstract1. Mechanisms underlying K +-induced hyperpolarizations in the presence and absence of phenylephrine were investigated in endothelium-denuded rat mesenteric arteries (for all mean values, n = 4). 2. Myocyte resting membrane potential (m.p.) was -58.8±0.8 mV. Application of 5 mM KCl produced similar hyperpolarizations in the absence (17.6±0.7 mV) or presence (15.8±1.0 mV) of 500 nM ouabain. In the presence of ouabain +30 μM barium, hyperpolarization to 5 mM KCl was essentially abolished. 3. In the presence of 10 μM phenylephrine (m.p. -33.7±3 mV), repolarization to 5 mM KCl did not occur in the presence or absence of 4-aminopyridine but was restored (-26.9±1.8 mV) on addition of iberiotoxin (100 nM). Under these conditions the K +-induced repolarization was insensitive to barium (30 μM) but abolished by 500 nm ouabain alone. 4. In the presence of phenylephrine + iberiotoxin the hyperpolarization to 5 mM K + was inhibited in the additional presence of 300 nM levcromakalim, an action which was reversed by 10 μM glibenclamide. 5. RT-PCR, Western blotting and immunohistochemical techniques collectively showed the presence of α 1-, α 2- and α 3-subunits of Na +/K +-ATPase in the myocytes. 6. In K +-free solution, re-introduction of K + (to 4.6 mM) hyperpolarized myocytes by 20.9±0.5 mV, an effect unchanged by 500 nM ouabain but abolished by 500 μM ouabain. 7. We conclude that under basal conditions, Na +/K +-ATPases containing α 2- and/or α 3-subunits are partially responsible for the observed K +-induced effects. The opening of myocyte K + channels (by levcromakalim or phenylephrine) creates a 'K + cloud' around the cells which fully activates Na +/K +-ATPase and thereby abolishes further responses to [K +] o elevation.
Persistent Identifierhttp://hdl.handle.net/10722/171274
ISSN
2015 Impact Factor: 5.259
2015 SCImago Journal Rankings: 2.368
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWeston, AHen_US
dc.contributor.authorRichards, GRen_US
dc.contributor.authorBurnham, MPen_US
dc.contributor.authorFélétou, Men_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorEdwards, Gen_US
dc.date.accessioned2012-10-30T06:13:06Z-
dc.date.available2012-10-30T06:13:06Z-
dc.date.issued2002en_US
dc.identifier.citationBritish Journal Of Pharmacology, 2002, v. 136 n. 6, p. 918-926en_US
dc.identifier.issn0007-1188en_US
dc.identifier.urihttp://hdl.handle.net/10722/171274-
dc.description.abstract1. Mechanisms underlying K +-induced hyperpolarizations in the presence and absence of phenylephrine were investigated in endothelium-denuded rat mesenteric arteries (for all mean values, n = 4). 2. Myocyte resting membrane potential (m.p.) was -58.8±0.8 mV. Application of 5 mM KCl produced similar hyperpolarizations in the absence (17.6±0.7 mV) or presence (15.8±1.0 mV) of 500 nM ouabain. In the presence of ouabain +30 μM barium, hyperpolarization to 5 mM KCl was essentially abolished. 3. In the presence of 10 μM phenylephrine (m.p. -33.7±3 mV), repolarization to 5 mM KCl did not occur in the presence or absence of 4-aminopyridine but was restored (-26.9±1.8 mV) on addition of iberiotoxin (100 nM). Under these conditions the K +-induced repolarization was insensitive to barium (30 μM) but abolished by 500 nm ouabain alone. 4. In the presence of phenylephrine + iberiotoxin the hyperpolarization to 5 mM K + was inhibited in the additional presence of 300 nM levcromakalim, an action which was reversed by 10 μM glibenclamide. 5. RT-PCR, Western blotting and immunohistochemical techniques collectively showed the presence of α 1-, α 2- and α 3-subunits of Na +/K +-ATPase in the myocytes. 6. In K +-free solution, re-introduction of K + (to 4.6 mM) hyperpolarized myocytes by 20.9±0.5 mV, an effect unchanged by 500 nM ouabain but abolished by 500 μM ouabain. 7. We conclude that under basal conditions, Na +/K +-ATPases containing α 2- and/or α 3-subunits are partially responsible for the observed K +-induced effects. The opening of myocyte K + channels (by levcromakalim or phenylephrine) creates a 'K + cloud' around the cells which fully activates Na +/K +-ATPase and thereby abolishes further responses to [K +] o elevation.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.subject4-Aminopyridineen_US
dc.subjectEdhfen_US
dc.subjectHyperpolarizationen_US
dc.subjectIberiotoxinen_US
dc.subjectImmuno-Histochemistryen_US
dc.subjectNa +/K +-Atpase Isoformsen_US
dc.subjectOuabainen_US
dc.subjectPhenylephrineen_US
dc.subjectPotassiumen_US
dc.titleK +-induced hyperpolarization in rat mesenteric artery: Identification, localization and role of Na +/K +-ATPasesen_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.0704787en_US
dc.identifier.pmid12110616-
dc.identifier.scopuseid_2-s2.0-0036022637en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036022637&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume136en_US
dc.identifier.issue6en_US
dc.identifier.spage918en_US
dc.identifier.epage926en_US
dc.identifier.isiWOS:000176947600013-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridWeston, AH=7102913361en_US
dc.identifier.scopusauthoridRichards, GR=7201583688en_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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