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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1 Pt 1
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pubmed:dateCreated |
1994-8-30
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pubmed:abstractText |
We determined the mechanisms by which beta-agonists increase sodium (Na+) currents across rat alveolar type II (ATII) cells grown in primary culture. When ATII cells were patched in the cell-attached mode using symmetrical Na+ solutions (150 mM Na(+)-glutamate), single-channel currents were observed for holding potentials between -80 and 30 mV (referenced to the pipette solution) with a single-channel conductance of 27 +/- 3 pS, a mean open time (tau 1) of 3.3 +/- 0.15 ms and an open probability (Po) of 0.36 +/- 0.06 (n = 7). Addition of 10 microM terbutaline into the bath increased tau 1 to 6.43 +/- 0.5 ms and Po to 0.62 +/- 0.06 (n = 7) without affecting channel conductance. Single-channel currents with a conductance of 25 +/- 2 pS were also recorded across ATII cells patched in the inside-out mode. Addition of 250 U/ml of protein kinase A (PKA), 1 mM ATP, and 5 mM MgCl2 in the bath solution (150 mM Na(+)-glutamate) increased the single channel tau 1 from 3.26 +/- 0.15 to 7.38 +/- 0.38 and Po from 0.41 +/- 0.06 to 0.72 +/- 0.07 (n = 6) without altering conductance. Addition of 1 microM amiloride or ethylisopropylamiloride (EIPA) in the pipette solution (150 mM Na(+)-glutamate) blocked single-channel activity almost completely. Ionic substitution experiments showed the relative permeability of Na+ to K+ and Na+ to Cl- to be 7:1 and 8:1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Amiloride,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins,
http://linkedlifedata.com/resource/pubmed/chemical/Plant Lectins,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Terbutaline,
http://linkedlifedata.com/resource/pubmed/chemical/ethylisopropylamiloride,
http://linkedlifedata.com/resource/pubmed/chemical/maclurin
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
267
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
L94-100
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8048548-Amiloride,
pubmed-meshheading:8048548-Animals,
pubmed-meshheading:8048548-Binding, Competitive,
pubmed-meshheading:8048548-Cells, Cultured,
pubmed-meshheading:8048548-Electrophysiology,
pubmed-meshheading:8048548-Lectins,
pubmed-meshheading:8048548-Macrophages, Alveolar,
pubmed-meshheading:8048548-Male,
pubmed-meshheading:8048548-Plant Lectins,
pubmed-meshheading:8048548-Pulmonary Alveoli,
pubmed-meshheading:8048548-Rats,
pubmed-meshheading:8048548-Rats, Sprague-Dawley,
pubmed-meshheading:8048548-Sodium Channels,
pubmed-meshheading:8048548-Terbutaline
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pubmed:year |
1994
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pubmed:articleTitle |
Regulation of low-amiloride-affinity sodium channels in alveolar type II cells.
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pubmed:affiliation |
Department of Anesthesiology, University of Alabama, Birmingham 35233.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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