Calmodulin kinase 2 activation is required for the maintenance of basal activity of L-type Ca[2+] channels in guinea-pig ventricular myocytes

DOI Web Site 被引用文献10件 参考文献77件
  • Hao Li-Ying
    Department of Pharmaceutical Toxicology, School of Pharmacological Sciences, China Medical University, China Department of Physiology, Graduate School of Medicine and Dental Sciences, Kagoshima University, Japan
  • Xu Jian-Jun
    Department of Physiology, Graduate School of Medicine and Dental Sciences, Kagoshima University, Japan
  • Minobe Etsuko
    Department of Physiology, Graduate School of Medicine and Dental Sciences, Kagoshima University, Japan
  • Kameyama Asako
    Department of Physiology, Graduate School of Medicine and Dental Sciences, Kagoshima University, Japan
  • Kameyama Masaki
    Department of Physiology, Graduate School of Medicine and Dental Sciences, Kagoshima University, Japan

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タイトル別名
  • Calmodulin Kinase II Activation Is Required for the Maintenance of Basal Activity of L-Type Ca<sup>2+</sup> Channels in Guinea-Pig Ventricular Myocytes
  • Calmodulin Kinase II Activation Is Required for the Maintenance of Basal Activity of L-Type Ca2+ Channels in Guinea-Pig Ventricular Myocytes

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The roles of calmodulin (CaM)-dependent protein kinase II (CaMKII) in the maintenance of basal activity and the reversion of run-down of L-type Ca2+ channels were studied in guinea-pig ventricular myocytes by the patch-clamp technique. In the cell-attached configuration, the Ca2+-channel activity was inhibited to 82% – 26% by 1 – 10 μM KN-93 and to 92% – 66% by 0.1 – 1 μM autocamtide-2–related inhibitory peptide (AIP) myristoylated. In the inside-out configuration, the bovine cardiac cytoplasm recovered Ca2+-channel activity to 87% of that recorded in the cell-attached configuration, while the CaMKII inhibitor 281-301 at 10 μM reduced the recovery effect to 19%. CaM + ATP recovered the channel activity to 93% and 28% of that recorded in the cell-attached configuration when applied at 1 and 5 min after run-down, respectively, showing a time-dependent attenuation. However, in the presence of 0.33 μM CaMKII, this attenuation was abolished, showing 85% and 75% recovery when applied at 1 and 5 min after run-down, respectively. This recovery effect was suppressed by 10 μM AIP, applied at 5 min, but not at 1 min after run-down. We concluded that CaMKII activation is required in the maintenance of basal activity of L-type Ca2+ channels.<br>

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