Intracellular regulation of Ca^<2+> release from cardiac sarcoplasmic reticulum.

我通过记录单通道电流，研究了心脏肌浆网离子通道的调节机制。(1)我发现心脏肌浆网（SR）中存在cl -通道，该通道被amp依赖性环磷酸化激活，并被Ca^<2+>/钙调蛋白复合物抑制。这是细胞内通道调控的新证据。我发表了关于这些证据的论文（Circulation Research, 1993）。(2) SR中的Ryanodine受体Ca^<2+>释放通道（RyR）对Ca^<2+>在细胞内的供应起重要作用。我们通过记录单通道活性来研究RyR的调控机制，发现蝎子毒素可以增强这些通道的开放，蝎子毒素可能是ryanodine受体的新型激活剂。Ca^<2+>拮抗剂维拉帕米直接阻断ryanodine受体通道开口，以减少心脏收缩。我展示了Mg^<2+>从SR中释放Ca^<2+>的详细调控机制。(2)细胞内Ca^<2+>由SR提供，在细胞功能中起着重要作用。我发现心脏肌膜具有Ca^<2+>激活的c1通道，并通过细胞内Ca^<2+>检查了该通道的详细激活机制。这篇论文目前在伦敦的《生理学杂志》上出版。我需要进一步研究这个cl通道的调控机制。

I have investigated the regulatory mechanism of ion channels in cardiac sarcoplasmic reticulum by recording single channel currents.(1) I found that Cl-channel existed in cardiac sarcoplasmic reticulum (SR) and that this channel was activated by cyclic AMP-dependent phosphorylation and was inhibited by Ca^<2+>/calmodulin complex. These are new evidences of intracellular channel regulations. I published the paper about these evidences (Circulation Research, 1993). (2) Ryanodine receptor Ca^<2+> release channel (RyR) in SR playd the important role for Ca^<2+> supply in the cells. We examined the regulatory mechanisms of RyR by recordingsingle channel activities and found that these channel openings were enhanced by scorpion toxin, which might be the new type of activator for ryanodine receptor. Ca^<2+> antagonist, verapamil, blocked ryanodine receptor channel openings directly to reduce the contraction of the heart. I showed the detail regulatory mechanisms of Ca^<2+> release from SR by Mg^<2+>.(2) Intracellular Ca^<2+> is supplied from SR and plays many important roles for cell functions. I found that cardiac sarcolemma had Ca^<2+> -activated C1-channel and examined the detail activation mechanisms of this channel by intracellular Ca^<2+>. This paper is now in press of Journal of Physiology in London. I need to study the further regulatory mechanisms of this Cl-channel.