| pubmed-article:8762072 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C0034493 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C1135918 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C0032718 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C0032821 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C0596019 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C0243077 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:8762072 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:8762072 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:8762072 | pubmed:dateCreated | 1997-2-14 | lld:pubmed |
| pubmed-article:8762072 | 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. | lld:pubmed |
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| pubmed-article:8762072 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8762072 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8762072 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8762072 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8762072 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:8762072 | pubmed:issn | 0007-1188 | lld:pubmed |
| pubmed-article:8762072 | pubmed:author | pubmed-author:LargeW AWA | lld:pubmed |
| pubmed-article:8762072 | pubmed:author | pubmed-author:TomaCC | lld:pubmed |
| pubmed-article:8762072 | pubmed:author | pubmed-author:HelliwellR... | lld:pubmed |
| pubmed-article:8762072 | pubmed:author | pubmed-author:GreenwoodI... | lld:pubmed |
| pubmed-article:8762072 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8762072 | pubmed:volume | 118 | lld:pubmed |
| pubmed-article:8762072 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8762072 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8762072 | pubmed:pagination | 513-20 | lld:pubmed |
| pubmed-article:8762072 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8762072 | pubmed:meshHeading | pubmed-meshheading:8762072-... | lld:pubmed |
| pubmed-article:8762072 | pubmed:year | 1996 | lld:pubmed |
| pubmed-article:8762072 | pubmed:articleTitle | Activation of potassium currents by inhibitors of calcium-activated chloride conductance in rabbit portal vein smooth muscle cells. | lld:pubmed |
| pubmed-article:8762072 | pubmed:affiliation | Department of Pharmacology and Clinical Pharmacology, St. George's Hospital Medical School, Cranmer Terrace, London. | lld:pubmed |
| pubmed-article:8762072 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8762072 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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