caa a22 4500 469078901 CHVBK 20180323132943.0 cr unu---uuuuu 170328e19920101xx s 000 0 eng 10.1007/BF00175473 doi (NATIONALLICENCE)springer-10.1007/BF00175473 Phenytoin partially antagonized L-type Ca2+ current in glucagon-secreting tumor cells (ITC-1) [Elektronische Daten] [T. Miyazaki, T. Hashiguchi, M. Hashiguchi, S. Sakai, T. Tosaka, M. Kanazawa] Summary: 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°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 α2 cells. Both currents were augmented by equimolar substitution of Ca2+ with Ba2+ and completely abolished by adding 1 μM 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 μM. The residual component of the L-type current was completely abolished by adding nifedipine. Springer-Verlag, 1992 ITC-1 cell nationallicence Low-threshold and transient Ca2+ (T-type) current nationallicence High-threshold and long-lasting Ca2+ (L-type) current nationallicence 5,5-diphenylhydantoin (phenytoin) nationallicence Miyazaki T. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut Hashiguchi T. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut Hashiguchi M. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut Sakai S. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut Tosaka T. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut Kanazawa M. Department of Internal Medicine, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/1(1992-01-01), 78-84 0028-1298 345:1<78 1992 345 210 https://doi.org/10.1007/BF00175473 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00175473 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Miyazaki T. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut NATIONALLICENCE 700 1- Hashiguchi T. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut NATIONALLICENCE 700 1- Hashiguchi M. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut NATIONALLICENCE 700 1- Sakai S. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut NATIONALLICENCE 700 1- Tosaka T. Department of Physiology, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut NATIONALLICENCE 700 1- Kanazawa M. Department of Internal Medicine, Tokyo Medical College, 6-1-1 Shinjuku, 160, Shinjuku-ku, Tokyo, Japan aut NATIONALLICENCE 773 0- Naunyn-Schmiedeberg's Archives of Pharmacology Springer-Verlag 345/1(1992-01-01), 78-84 0028-1298 345:1<78 1992 345 210 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer