Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-7-19
pubmed:abstractText
1. To investigate the role of long-term stimulation of nicotinic acetylcholine receptors (AChRs) on the regulation of membrane potential, non-contracting C2C12 myotubes were stimulated for 1-4 days with carbachol (10 microM) and membrane potentials were measured by the intracellular microelectrode technique after washing out of the drug. 2. The membrane potential (-45.7 mV) gradually increased by 10.1 mV to -55.8 mV during 4 days treatment, which was caused by enhanced electrogenic Na+/K(+)-pumping. 3. The concentration-dependent enhancement of Na+/K(+)-ATPase activity in long-term carbachol-treated myotubes (4 days, EC50 = 5.3 microM) was prevented by co-treatment with the competitive nicotinic AChR antagonist, pancuronium but not by the muscarinic antagonist, atropine. 4. Enhanced Na+/K(+)-ATPase activity still developed in carbachol-stimulated myotubes during co-treatment (4 days) with the nicotinic AChR-channel blocker, chlorpromazine (1 microM). Membrane depolarization as such, obtained by incubation in high K+ medium (40 mM, 4 days) did not enhance Na+/K(+)-ATPase activity. 5. Non-treated myotubes possessed a high-affinity ouabain binding site (Kd = 119 nM) in association with the low Na+/K(+)-pumping activity. Long-term stimulation of myotubes (4 days) with carbachol or with a combination of carbachol and chlorpromazine was accompanied by the development of an additional low-affinity ouabain binding site (Kd = 13 microM). 6. Binding of monoclonal antibodies directed against either alpha 1- or alpha 2-subunit of Na+/K(+)-ATPase were both increased in myotubes treated with carbachol (4 days). 7. These results support the concept that nicotinic AChRs regulate Na+/K(+)-ATPase activity, independent of the functionality of the receptor-operated ion-channel.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-1331053, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-1393284, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-1592722, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-166159, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-1689313, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-170397, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-2080554, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-2176238, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-2455720, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-2541792, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-2542271, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-2579711, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-3015915, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-4171017, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-5032352, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-563524, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-6254391, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-6254793, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-6373449, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-64930, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-722508, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-839441, http://linkedlifedata.com/resource/pubmed/commentcorrection/8004390-8469610
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0007-1188
pubmed:author
pubmed:issnType
Print
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
459-64
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Induction of Na+/K(+)-ATPase activity by long-term stimulation of nicotinic acetylcholine receptors in C2C12 myotubes.
pubmed:affiliation
Department of Pharmacology/Clinical Pharmacology, University of Groningen, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't