Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-5-6
pubmed:abstractText
Large-conductance Ca2(+)-activated K+ channels were studied in membranes of cultured rabbit airway smooth muscle cells, using the patch-clamp technique. In cell-attached recordings, channel openings were rare and occurred only at very positive potentials. Bradykinin (10 microM), an agonist which releases Ca2+ from the sarcoplasmic reticulum, transiently increased channel activity. The metabolic blocker 2,4-dinitrophenol (20 microM), which lowers cellular adenosine triphosphate (ATP) levels, induced a sustained increase of channel activity in cell-attached patches. In excised patches, these channels had a slope conductance of 155 pS at 0 mV, were activated by depolarization and by increasing the Ca2+ concentration at the cytoplasmic side above 10(-7) mol/l. ATP, applied to the cytoplasmic side of the patches, dose-dependently decreased the channel's open-state probability. An inhibition constant (Ki) of 0.2 mmol/l was found for the ATP-induced inhibition. ATP reduced the Ca2+ sensitivity of the channel, shifting the Ca2+ activation curve to the right and additionally reducing its steepness. Our results demonstrate that cytoplasmic ATP inhibits a large-conductance Ca2(+)-activated K+ channel in airway smooth muscle. This ATP modulation of Ca2(+)-activated K+ channels might serve as an important mechanism linking energy status and the contractile state of the cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
417
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
517-22
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Ca2(+)-activated K+ channels in airway smooth muscle are inhibited by cytoplasmic adenosine triphosphate.
pubmed:affiliation
University of Miami, School of Medicine, Department of Molecular and Cellular Pharmacology, FL 33101.
pubmed:publicationType
Journal Article