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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1997-2-14
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pubmed:abstractText |
1. The conventional whole-cell recording technique was used to study the effects of the chloride channel inhibitors ethacrynic acid, anthracene-9-carboxylic acid (A-9-C) and indanyloxyacetic acid (IAA) on membrane currents in rabbit portal vein smooth muscle cells at a holding potential of 0 mV. 2. Using a pipette solution that contained 1 x 10(-4) M 1,2-bis (2-aminophenoxy)-ethane-N,N,N,N,-tetraacetic acid (BAPTA) and a normal bathing solution the addition of ethacrynic acid (2 x 10(-4) M to 1 x 10(-3) M) inhibited spontaneous transient outward currents (STOCs) and evoked a concentration-dependent current at a holding potential of 0 mV. A similar current was activated by IAA (5 x 10(-4) M to 1 x 10(-3) M) but not by A-9-C (1-5 x 10(-3) M) at a holding potential of 0 mV. 3. The amplitude of the current evoked by ethacrynic acid and IAA was linearly related to potential between -30 and 0 mV and displayed outward rectification at positive potentials. The current induced by A-9-C was evident only at potentials positive to +20 mV. 4. Glibenclamide (1 x 10(-5) M) abolished the current evoked by ethacrynic acid and IAA at potentials negative to +10 mV and partially inhibited the current positive to +10 mV. The glibenclamide-insensitive current at positive potentials was completely inhibited by 1 x 10(-3) M TEA. The A-9-C-evoked current was insensitive to glibenclamide and abolished by 1 x 10(-3) M TEA. 5. The glibenclamide-sensitive current activated by ethacrynic acid was not sustained and declined to control levels in the continued presence of ethacrynic acid. However, the outwardly rectifying current recorded at +50 mV was well maintained over the same period. 6. Outwardly rectifying currents evoked by ethacrynic acid and A-9-C were observed with a pipette solution containing 1 x 10(-2) M BAPTA in cells bathed in Ca-free extracellular solution containing 5 x 10(-4) M BAPTA and 1 x 10(-5) M cyclopiazonic acid. 7. It is concluded that all three chloride-channel blockers activated an outwardly rectifying, TEA-sensitive current. Moreover, ethacrynic acid and IAA evoked an additional glibenclamide-sensitive current which was present at all potentials between -30 and +50 mV.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-1330156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-1467843,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-1504756,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-1900393,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-2442706,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-2600838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-2621620,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-7534190,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-7535111,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-7685635,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-7735693,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-7921628,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-7965736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8032620,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8137869,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8242231,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8242233,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8548170,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8564233,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8762072-8680728
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0007-1188
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
118
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
513-20
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8762072-Animals,
pubmed-meshheading:8762072-Chloride Channels,
pubmed-meshheading:8762072-Dose-Response Relationship, Drug,
pubmed-meshheading:8762072-Egtazic Acid,
pubmed-meshheading:8762072-Ethacrynic Acid,
pubmed-meshheading:8762072-Female,
pubmed-meshheading:8762072-Membrane Potentials,
pubmed-meshheading:8762072-Muscle, Smooth, Vascular,
pubmed-meshheading:8762072-Portal Vein,
pubmed-meshheading:8762072-Potassium Channels,
pubmed-meshheading:8762072-Rabbits
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pubmed:year |
1996
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pubmed:articleTitle |
Activation of potassium currents by inhibitors of calcium-activated chloride conductance in rabbit portal vein smooth muscle cells.
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pubmed:affiliation |
Department of Pharmacology and Clinical Pharmacology, St. George's Hospital Medical School, Cranmer Terrace, London.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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