| pubmed-article:9151659 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0003308 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0023440 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0009074 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0949653 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0870883 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0205164 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0020923 | lld:lifeskim |
| pubmed-article:9151659 | lifeskim:mentions | umls-concept:C0591833 | lld:lifeskim |
| pubmed-article:9151659 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:9151659 | pubmed:dateCreated | 1997-6-23 | lld:pubmed |
| pubmed-article:9151659 | pubmed:abstractText | Clotrimazole (CLT), a member of the antifungal imidazole family of compounds, has been found to inhibit both calcium (Ca2+)-activated 86Rb and potassium (K) fluxes of human red cells and to inhibit red cell binding of 125I-charybdotoxin (ChTX) [11]. We have now used patch-clamp techniques to demonstrate reversible inhibition of whole cell KCa2+ currents in murine erythroleukemia (MEL) cells by submicromolar concentrations of CLT. Inhibition was equivalent whether currents were elicited by bath application of the Ca2+ ionophore A23187 or by dialyzing cells with a pipette solution containing micromolar concentrations of free Ca2+. The extent of inhibition of whole cell MEL KCa2+ currents was voltage-dependent, decreasing with increasing test potential. We also determined the single channel basis of the CLT inhibition in MEL cells by demonstrating the inhibition of a calcium-activated, ChTX-sensitive K channel by CLT in outside-out patches. The channel was also blocked by the des-imidazolyl metabolite of CLT, 2-chlorophenyl-bisphenyl-methanol (MET II) [15], thus demonstrating that the imidazole ring is not required for the inhibitory action of CLT. Single KCa2+ channels were also evident in inside-out patches of MEL cells. Block of K current by CLT was not unique to MEL cells. CLT also inhibited a component of the whole cell K current in PC12 cells. Channel specificity of block by CLT was determined by examining its effects on other types of voltage-sensitive currents. CLT block showed the following rank order of potency: K currents in PC12 cells > Ca2+ currents in PC12 cells >> Na currents in sympathetic neurons. These results demonstrate that direct inhibition of single KCa2+ by CLT can be dissociated from inhibition of cytochrome P-450 in MEL cells. | lld:pubmed |
| pubmed-article:9151659 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9151659 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9151659 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9151659 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9151659 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9151659 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9151659 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9151659 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9151659 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9151659 | pubmed:month | May | lld:pubmed |
| pubmed-article:9151659 | pubmed:issn | 0022-2631 | lld:pubmed |
| pubmed-article:9151659 | pubmed:author | pubmed-author:AlperS LSL | lld:pubmed |
| pubmed-article:9151659 | pubmed:author | pubmed-author:BrugnaraCC | lld:pubmed |
| pubmed-article:9151659 | pubmed:author | pubmed-author:VandorpeD HDH | lld:pubmed |
| pubmed-article:9151659 | pubmed:author | pubmed-author:RittenhouseA... | lld:pubmed |
| pubmed-article:9151659 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9151659 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:9151659 | pubmed:volume | 157 | lld:pubmed |
| pubmed-article:9151659 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9151659 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9151659 | pubmed:pagination | 177-91 | lld:pubmed |
| pubmed-article:9151659 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:9151659 | pubmed:meshHeading | pubmed-meshheading:9151659-... | lld:pubmed |
| pubmed-article:9151659 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9151659 | pubmed:articleTitle | The antifungal imidazole clotrimazole and its major in vivo metabolite are potent blockers of the calcium-activated potassium channel in murine erythroleukemia cells. | lld:pubmed |
| pubmed-article:9151659 | pubmed:affiliation | Molecular Medicine & Renal Units, Beth Israel Hospital, 330 Brookline Ave., Boston, MA 02215, USA. | lld:pubmed |
| pubmed-article:9151659 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9151659 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:9151659 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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