| pubmed-article:7520693 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7520693 | lifeskim:mentions | umls-concept:C0076374 | lld:lifeskim |
| pubmed-article:7520693 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:7520693 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:7520693 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:7520693 | lifeskim:mentions | umls-concept:C0056801 | lld:lifeskim |
| pubmed-article:7520693 | pubmed:dateCreated | 1994-9-21 | lld:pubmed |
| pubmed-article:7520693 | pubmed:abstractText | Thapsigargin (TG), 2,5-t-butylhydroquinone (tBHQ) and cyclopiazonic acid (CPA) all inhibit the initial Ca(2+)-response to thyrotropin-releasing hormone (TRH) by depleting intracellular Ca2+ pools sensitive to inositol 1,4,5-trisphosphate (IP3). Treatment of GH3 pituitary cells for 30 min with 5 nM TG, 500 nM tBHQ or 50 nM CPA completely eliminated the TRH-induced spike in intracellular free Ca2+ ([Ca2+]i). Higher concentrations of TG and tBHQ, but not CPA, were also found to inhibit strongly the activity of L-type calcium channels, as measured by the increase in [Ca2+]i or 45Ca2+ influx stimulated by depolarization. TG and tBHQ blocked high-K(+)-stimulated 45Ca2+ uptake, with IC50 values of 10 and 1 microM respectively. Maximal inhibition of L-channel activity was achieved 15-30 min after drug addition. Inhibition by tBHQ was reversible, whereas inhibition by TG was not. TG and CPA did not affect spontaneous [Ca2+]i oscillations when tested at concentrations adequate to deplete the IP3-sensitive Ca2+ pool. However, 20 microM TG and 10 microM tBHQ blocked [Ca2+]i oscillations completely. The effect of drugs on calcium currents was measured directly by using the patch-clamp technique. When added to the external bath, 10 microM CPA caused a sustained increase in the calcium-channel current amplitude over 8 min, 10 microM tBHQ caused a progressive inhibition, and 10 microM TG caused an enhancement followed by a sustained block of the calcium current over 8 min. In summary, CPA depletes IP3-sensitive Ca2+ stores and does not inhibit voltage-operated calcium channels. At sufficiently low concentrations, TG depletes IP3-sensitive stores without inhibiting L-channel activity, but, for tBHQ, inhibition of calcium channels occurs at concentrations close to those needed to block agonist mobilization of intracellular Ca2+. | lld:pubmed |
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| pubmed-article:7520693 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7520693 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7520693 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7520693 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:7520693 | pubmed:issn | 0264-6021 | lld:pubmed |
| pubmed-article:7520693 | pubmed:author | pubmed-author:LiC CCC | lld:pubmed |
| pubmed-article:7520693 | pubmed:author | pubmed-author:HinkleP MPM | lld:pubmed |
| pubmed-article:7520693 | pubmed:author | pubmed-author:KassR SRS | lld:pubmed |
| pubmed-article:7520693 | pubmed:author | pubmed-author:BensowCC | lld:pubmed |
| pubmed-article:7520693 | pubmed:author | pubmed-author:NelsonE JEJ | lld:pubmed |
| pubmed-article:7520693 | pubmed:author | pubmed-author:BangaloreRR | lld:pubmed |
| pubmed-article:7520693 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7520693 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7520693 | pubmed:volume | 302 ( Pt 1) | lld:pubmed |
| pubmed-article:7520693 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7520693 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7520693 | pubmed:pagination | 147-54 | lld:pubmed |
| pubmed-article:7520693 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:7520693 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:7520693 | pubmed:articleTitle | Inhibition of L-type calcium-channel activity by thapsigargin and 2,5-t-butylhydroquinone, but not by cyclopiazonic acid. | lld:pubmed |
| pubmed-article:7520693 | pubmed:affiliation | Department of Pharmacology, University of Rochester School of Medicine and Dentistry, NY 14642. | lld:pubmed |
| pubmed-article:7520693 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7520693 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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