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モルモット肝細胞内acidosisの細胞膜K^+ channelに与える影響
https://kindai.repo.nii.ac.jp/records/2002009
https://kindai.repo.nii.ac.jp/records/200200983be0d9a-c089-486f-8e66-d6879fd20c62
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00063584-19940325-0153.pdf (528.3 KB)
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| Item type | ☆紀要論文 / Departmental Bulletin Paper(1) | |||||||||
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| 公開日 | 2024-11-15 | |||||||||
| タイトル | ||||||||||
| タイトル | モルモット肝細胞内acidosisの細胞膜K^+ channelに与える影響 | |||||||||
| 言語 | ja | |||||||||
| タイトル | ||||||||||
| タイトル | Effects of intracellular acidification on K^+ channel in guinea pig hepatocytes | |||||||||
| 言語 | en | |||||||||
| 著者 |
別所, 偉光
× 別所, 偉光
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| 言語 | ||||||||||
| 言語 | jpn | |||||||||
| キーワード | ||||||||||
| 主題 | patch clamp, K^+ channel, quinidine, apamin, Na^+-H^+ exchange, acidosis | |||||||||
| 資源タイプ | ||||||||||
| 資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||||||
| 資源タイプ | departmental bulletin paper | |||||||||
| 出版タイプ | ||||||||||
| 出版タイプ | AM | |||||||||
| 出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||||||
| 出版者 名前 | ||||||||||
| 出版者 | 近畿大学医学会 | |||||||||
| 言語 | ja | |||||||||
| bibliographic_information |
ja : 近畿大学医学雑誌 en : Medical Journal of Kinki University 巻 19, 号 1, p. 153-165, 発行日 1994-03-25 |
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| ISSN | ||||||||||
| 収録物識別子タイプ | PISSN | |||||||||
| 収録物識別子 | 03858367 | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Abstract | |||||||||
| 内容記述 | Both the whole cell patch clamp technique and single channel recording were used to investigate the voltage dependent outward current in enzymatically dissociated guinea pig hepatocytes. A voltage-gated outward current with an outward rectifier component was observed. The single channel behavior of this channel was also studied. The delayed rectifying outward current was activated at membrane potentials over-10 mV. More pronounced effect was seen at more positive depolarizing potentials under both whole cell patch clamp mode and single channel recordings. That is, with a patch attached to the cell and with +40 mV depolarizing pulses from RP-20 mV, slow inactivating channel activities were observed. After external application of 20 μM quinidine under conditions of cell attached patch, or after external application of 0.1 μM apamin under conditions of whole cell patch clamp, the outward component was reversibly blocked under conditions of both whole cell and single channel patch clamp techniques. Furthermore, after external application of 1 mM nicorandil, the outward component increased under conditions of whole cell patch clamp techniques, supporting the hypothesis that this current component belongs to the K^+ channel. When the pH in the external solution was changed from 7.2 to 6.2, the K^+ current was not inhibited with extracellular acidosis. When the pH in the pipette solution was changed from 7.2 to 6.2 the K^+ current was significantly inhibited. Therefore, we assume that some kind of buffer system is involved in the hepatocytes. The presence of a K^+ channel and Na^+-H^+ exchange mechanism was clarified in guinea pig hepatocytes and the mechanism responded to intracellular acidification to a clinical significance. | |||||||||
| 言語 | en | |||||||||
| 内容記述 | ||||||||||
| 内容記述タイプ | Other | |||||||||
| 内容記述 | 本文データはCiNiiから複製したものである。 | |||||||||
| 言語 | ja | |||||||||
