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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1993-1-11
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pubmed:abstractText |
The selective alpha 1-adrenergic agonist methoxamine (10(-4)-10(-3) M), in the presence of propranolol (10(-6) M), can reduce both the inwardly rectifying K+ background current (IK1) and the muscarinic cholinergic receptor-activated K+ current (IK,ACh) in rabbit atrial myocytes resulting in action potential prolongation during the final phase of repolarization and a depolarization of the resting membrane potential. The reduction of these K+ currents(s) by alpha 1-adrenoceptor stimulation was insensitive to pre-treatment of atrial myocytes with pertussis toxin (0.15-0.5 micrograms/ml) and was irreversible following intracellular dialysis with the non-hydrolysable guanosine triphosphate (GTP) analogue, Gpp(NH)p (1-5 x 10(-3) M). Neither the protein kinase C (PKC) inhibitors, 1((5-isoquinolinesulphonyl)-2-methylpiperoxine (H-7) (5 x 10(-5) M) and staurosporine (1 x 10(-7) M), nor "downregulation" of PKC by prolonged phorbol ester exposure (5 x 10(-7) M, for 7-8 h) had an effect on the alpha 1-adrenergic modulation of this K+ current. Under cell-attached patch-clamp conditions, bath application of methoxamine reversibly decreased acetylcholine-induced single-channel activity, thus confirming the observed reduction of the ACh-induced current under whole-cell voltage clamp. These results demonstrate that the alpha 1-adrenoceptor, once activated, can reduce current through two different inwardly rectifying K+ channels in rabbit atrial myocytes. These current changes are mediated via a pertussis toxin-insensitive GTP-binding protein, and do not appear to involve the activation of PKC.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic alpha-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/GTP-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Guanosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Methoxamine,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0031-6768
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
421
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
431-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1361052-Action Potentials,
pubmed-meshheading:1361052-Adrenergic alpha-Agonists,
pubmed-meshheading:1361052-Animals,
pubmed-meshheading:1361052-Cells, Cultured,
pubmed-meshheading:1361052-Down-Regulation,
pubmed-meshheading:1361052-GTP-Binding Proteins,
pubmed-meshheading:1361052-Guanosine Triphosphate,
pubmed-meshheading:1361052-Heart Atria,
pubmed-meshheading:1361052-Methoxamine,
pubmed-meshheading:1361052-Myocardium,
pubmed-meshheading:1361052-Potassium Channels,
pubmed-meshheading:1361052-Rabbits
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pubmed:year |
1992
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pubmed:articleTitle |
Activation of alpha 1-adrenoceptors modulates the inwardly rectifying potassium currents of mammalian atrial myocytes.
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pubmed:affiliation |
Department of Medical Physiology and Medicine, University of Calgary, Alberta, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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