第17回 日本心電学会サテライト国際シンポジウム

• Nakaya Haruaki

  Department of Pharmacology, Chiba University School of Medicine

• Suzuki Masashi

  Department of Pharmacology, Chiba University School of Medicine

• Uemura Hiroko

  Department of Pharmacology, Chiba University School of Medicine

• Sakamoto Naoya

  Department of Pharmacology, Chiba University School of Medicine

• Ohmoto Yuki

  Department of Pharmacology, Chiba University School of Medicine

• Ogura Takehiko

  Department of Pharmacology, Chiba University School of Medicine

• Tamagawa Masaji

  Department of Pharmacology, Chiba University School of Medicine

• Furusawa Yoshie

  Department of Pharmacology, Chiba University School of Medicine

• Sakashita Ikumi

  Department of Pharmacology, Chiba University School of Medicine

• Suzuki Toshio

  Department of Pharmacology, Chiba University School of Medicine

• Miki Takashi

  Department of Molecular Medicine, Chiba University Graduate School of Medicine

• Seino Susumu

  Department of Molecular Medicine, Chiba University Graduate School of Medicine

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”
• Sarcolemmal ATP-sensitive K<SUP>+</SUP> channels and cardiovascular function

抄録

Recent studies have demonstrated that ATP-sensitive K⁺ (K_ATP) channel is a complex of the inwardly rectifying K⁺ channel subfamily Kir6.0 and the receptors for sulfonylureas (SUR) . It is well established that K_ATP channel in pancreatic β cell is composed of Kir6.2 and SUR1. However, functional molecules of K_ATP channels in cardiovascular tissues have not been determined. Recent studies h ave s u gge ste d th at cardi oprote ctive effect of K⁺ channel openers or ischemic preconditioning is mediated by the activation of mitochondrial K_ATP channels, another type of K_ATP channel whose molecular structure is still undefined. Therefore, it would be important to determine the role of sarcolemmal K_ATP channel in cardiac cells. Recently K_ATP channel-deficient mice were generated by genetic disruption of Kir6.2. The Kir6.2-deficient mice may be useful for the evaluation of functional roles of sarcolemmal K_ATP channels in cardiovascular tissues. In this review, we describe present understanding of molecular structure and physiological roles of sarcolemmal K_ATP channels in cardiovascular tissues.

収録刊行物

• 心電図

  心電図 20 (Suppl3), 113-116, 2000

  一般社団法人　日本不整脈心電学会

詳細情報

• CRID: 1390001204772139520
• NII論文ID: 10008114203
• NII論文ID: 130004087458
• NII書誌ID: AN00358282
• DOI: 10.5105/jse.20.suppl3_113
• ISSN: 18842437
• ISSN: 02851660
• 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