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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1989-3-23
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pubmed:abstractText |
Although there is compelling pharmacological evidence based on Ca2+-channel antagonist studies suggesting that the voltage-dependent Ca2+ channels regulate insulin release, no direct comparison with Ca2+ currents exists. This is particularly important because of the recent demonstration in other cell types of one and possibly two Ca2+ channels that are insensitive to Ca2+-channel antagonists, the dihydropyridines and the phenylalkylamines. Using an SV40-transformed pancreatic beta-cell line (HIT cells), we determined how voltage-dependent Ca2+ channels are involved in stimulus-secretion coupling. Ca2+ currents were measured with the tight-seal technique for whole-cell recording. The cytosolic free-Ca2+ concentration ([Ca2+]i) was followed with the fluorescent probe Fura 2, and the measurements were compared with insulin secretion stimulated by depolarizing the cells with K+. The Ca2+ current contained two components: a rapidly decaying current activated at -50 to -40 mV that decayed with a time constant of 25 ms and a very slowly decaying component activated at -40 mV. Both components were sensitive to the Ca2+-channel antagonist nimodipine. There is excellent agreement in the concentration of nimodipine that inhibited Ca2+ and the increase in [Ca2+]i in response to K+ depolarization (IC50 of 15 and 6 nM, respectively). Nimodipine inhibited insulin release over a similar dose-response range with an IC50 of 1.5 x 10(-9) M. These studies indicate that the increase in [Ca2+]i in response to beta-cell depolarization can be accounted for by the influx of this ion through a single class of dihydropyridine-sensitive Ca2+ channels in the cell membrane.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Barium,
http://linkedlifedata.com/resource/pubmed/chemical/Benzofurans,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Fura-2,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Nimodipine,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0012-1797
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
38
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
188-93
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:2536627-Animals,
pubmed-meshheading:2536627-Barium,
pubmed-meshheading:2536627-Benzofurans,
pubmed-meshheading:2536627-Calcium,
pubmed-meshheading:2536627-Calcium Channels,
pubmed-meshheading:2536627-Cell Line,
pubmed-meshheading:2536627-Cytosol,
pubmed-meshheading:2536627-Fura-2,
pubmed-meshheading:2536627-Insulin,
pubmed-meshheading:2536627-Islets of Langerhans,
pubmed-meshheading:2536627-Membrane Potentials,
pubmed-meshheading:2536627-Nimodipine,
pubmed-meshheading:2536627-Potassium
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pubmed:year |
1989
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pubmed:articleTitle |
Characterization of voltage-dependent Ca2+ channels in beta-cell line.
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pubmed:affiliation |
Department of Physiology and Molecular Biophysics, Baylor College of Medicine, Houston, Texas 77030.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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