An electrophysiological study on miniature Ca relelase from the sarcoplasmic reticulum in cardiac myocytes.

摘要。为了研究细胞内Ca^<2+>水平升高对细胞膜电活动的影响，在全细胞记录的条件下，将促进肌浆网Ca^<2+>释放的药物咖啡因应用于豚鼠单心室细胞。咖啡因（10 - 25mm）引起脉冲状的小电流向内爆发。当膜去极化时，脉冲状向内电流的幅值逐渐减小，其反转电位估计在0 mV附近。因此，离子通道的单位电导可能在250 ~ 300 pS之间。当外部NaCl被LiCl取代时，脉冲样活性仍然存在，但在Tris-Cl溶液中消失。大的去极化产生持续的细胞缩短或细胞内Ca^<2+>注射增强了脉冲样事件，表明细胞内Ca^<2+>在这一现象中起作用。Ni^<2+>离子部分抑制了脉冲样活性。因此，心室细胞似乎具有Ca^<2+>介导的具有大电导的阳离子通道，但不排除咖啡因在通道激活中的特定作用。

Abstract. In order to examine the effects of increased intracellular Ca^<2+> level on the membrane electrical activity, caffeine, the agent which facilitates Ca^<2+> release from the sarcoplasmic reticulum, was applied to single ventricular cells of the guinea-pig, under condition of the whole cell recording. Caffeine (10 - 25 mM) induced a burst of pulse-like small inward currents. The amplitude of the pulse-like inward currents, which appeared to have a unit magnitude, decreased as the membrane was depolarized, and the reversal potential was estimated to be near 0 mV. Thus, the responsible ion channel may have a unit conductance of 250 - 300 pS. The pulse-like activity persisted when external NaCl was replaced with LiCl, but it disappeared in Tris-Cl solution. Large depolarizations producing sustained cell shortening or intracellular Ca^<2+>-injection enhanced the pulse-like events, suggesting a role of intracellular Ca^<2+> in this phenomenon. Ni^<2+> ions partially inhibited the pulse-like activity. Thus, the ventricular cells appeared to have Ca^<2+>-mediated cation channels with a large conductance, but possible involvement of a specific action of caffeine in the channel activation was not excluded.