第17回 日本心電学会サテライト国際シンポジウム

• Ono Katsushige

  Department of Physiology, Oita Medical University

• Lee Tae-Seong

  Department of Physiology, Oita Medical University

• Kaku Toshihiko

  Department of Physiology, Oita Medical University

• Arita Makoto

  Department of Physiology, Oita Medical University

書誌事項

タイトル別名

• Oita International Electrocardiology Symposium 2000 “Electrophysiology and Management of Lethal Arrhythmias in the New Millennium: From Genes to Bedside”
• Pharmacological properties of the human cardiac cloned T-type calcium channel

抄録

The effects of calcium (Ca²⁺) channel antagonists on the T-type Ca²⁺ channel current were investigated in Human Embryonic Kidney (HEK-293) cells heterologously expressing the a subunit of the human cardiac T-type Ca²⁺ channel. Ca²⁺ current were elicited by depolarization in 1.8 mM Ca²⁺ and recorded in the whole-cell configuration of the patch-clamp technique. The T-type Ca²⁺ current was inhibited by the following calcium channel antagonists: mibefradil (IC₅₀=0.89μM), efonidipine (IC₅₀=0.43μM) and nifedipine (IC₅₀=1.91μM) . However, the agents differed in the use dependence of their effects. Mibefradil and efonidipine exhibit a strong use-dependent inhibition of the current that is due to selective interaction with the open state and the inactivated state of the channel, rather than with the resting state. Voltage dependence of inactivation and activation were modified in the presence of these agents: both curves were shifted in the hyperpolarized potentials by 5-10 mV by application of these Ca²⁺ channel antagonists at the concentration of IC50, respectively.

収録刊行物

• 心電図

  心電図 20 (Suppl3), 109-112, 2000

  一般社団法人　日本不整脈心電学会

詳細情報

• CRID: 1390282679748851584
• NII論文ID: 10008114192
• NII論文ID: 130004087456
• NII書誌ID: AN00358282
• DOI: 10.5105/jse.20.suppl3_109
• ISSN: 18842437
• ISSN: 02851660
• ISSN: http://id.crossref.org/issn/00220736
• データソース種別:
  • JaLC
  • Crossref
  • CiNii Articles
• 抄録ライセンスフラグ: 使用不可