| pubmed-article:1311428 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1311428 | lifeskim:mentions | umls-concept:C0431085 | lld:lifeskim |
| pubmed-article:1311428 | lifeskim:mentions | umls-concept:C0031507 | lld:lifeskim |
| pubmed-article:1311428 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:1311428 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:1311428 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1311428 | pubmed:dateCreated | 1992-4-2 | lld:pubmed |
| pubmed-article:1311428 | pubmed:abstractText | Transmembrane Ca2+ currents were investigated by means of a whole-cell clamp technique in a hamster glucagon-secreting tumor cell line (ITC-1). Two types of Ca2+ current were identified in ITC-1 cells. The low-threshold and transient (T-type) current became detectable above the potential level around -60 mV and decayed rapidly with an inactivation time constant of 95 ms (at -40 mV and 23 degrees C), while the high-threshold and long-lasting (L-type) one was activated by depolarization more positive to -30 mV with non-inactivating kinetics. The voltage dependence and kinetics of these currents were identical to those reported in guinea-pig pancreatic alpha 2 cells. Both currents were augmented by equimolar substitution of Ca2+ with Ba2+ and completely abolished by adding 1 microM La3+. Phenytoin, a well known anti-epileptic drug and a postulated T-type specific Ca2+ current antagonist, surprisingly blocked the L-type current without affecting the T-type current in ITC-1 cells. While phenytoin antagonized the L-type Ba2+ current selectively, 60% of the current remained even in supramaximal concentration range over 500 microM. The residual component of the L-type current was completely abolished by adding nifedipine. | lld:pubmed |
| pubmed-article:1311428 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1311428 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1311428 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1311428 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:1311428 | pubmed:issn | 0028-1298 | lld:pubmed |
| pubmed-article:1311428 | pubmed:author | pubmed-author:SakaiSS | lld:pubmed |
| pubmed-article:1311428 | pubmed:author | pubmed-author:MiyazakiTT | lld:pubmed |
| pubmed-article:1311428 | pubmed:author | pubmed-author:TosakaTT | lld:pubmed |
| pubmed-article:1311428 | pubmed:author | pubmed-author:HashiguchiTT | lld:pubmed |
| pubmed-article:1311428 | pubmed:author | pubmed-author:KanazawaMM | lld:pubmed |
| pubmed-article:1311428 | pubmed:author | pubmed-author:HashiguchiMM | lld:pubmed |
| pubmed-article:1311428 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1311428 | pubmed:volume | 345 | lld:pubmed |
| pubmed-article:1311428 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1311428 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1311428 | pubmed:pagination | 78-84 | lld:pubmed |
| pubmed-article:1311428 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:meshHeading | pubmed-meshheading:1311428-... | lld:pubmed |
| pubmed-article:1311428 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1311428 | pubmed:articleTitle | Phenytoin partially antagonized L-type Ca2+ current in glucagon-secreting tumor cells (ITC-1). | lld:pubmed |
| pubmed-article:1311428 | pubmed:affiliation | Department of Physiology, Tokyo Medical College, Japan. | lld:pubmed |
| pubmed-article:1311428 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1311428 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:1311428 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
