Nemoto K, Okamura T
Department of Pharmacology, Nippon Medical School.
Arerugi. 1994 Jan;43(1):44-54.
Tracheal muscle strips isolated from guinea pigs passively sensitized with anti-egg albumin rabbit IgG were loaded with 86Rb as a K+ marker. The 86Rb efflux from the muscle tissue was measured after antigen exposure and the K(+)-channel subtypes involved in anaphylactic contraction were identified. The net 86Rb efflux was increased during antigen challenge. This increase was inhibited in Ca(2+)-free medium or in the medium of 40 mM of KCl, but not by 10 microM of glibenclamide or 20 mM of KCl. Decreased membrane potential and generation of action potentials were also observed during the anaphylactic contraction. As a comparison for antigen-induced 86Rb efflux changes, experiments using high concentrations of KCl were also performed. 86Rb efflux was increased depending on the KCl concentration. This increase was inhibited in Ca(2+)-free medium but not by 10 microM of glibenclamide. These results suggest that the K(+)-channel opening during IgG-mediated anaphylactic contraction was dependent on a decreased membrane potential due to 20-40 mM KCl. The subtype of the K(+)-channel involved is voltage-dependent K(+)-channel (Kv-channel), and Ca(2+)-activated K(+)-channel (KCa-channel) may also be involved in the 86Rb efflux change. The ATP-sensitive K(+)-channel (KATP-channel) was not involved in K(+)-channel opening during anaphylactic contraction.
从用抗卵清蛋白兔IgG被动致敏的豚鼠中分离出气管肌条，用⁸⁶Rb作为钾离子标记物进行负载。在抗原暴露后测量肌肉组织中⁸⁶Rb的流出，并鉴定参与过敏反应性收缩的钾离子通道亚型。在抗原攻击期间，⁸⁶Rb的净流出增加。这种增加在无钙培养基或40 mM氯化钾的培养基中受到抑制，但不受10 μM格列本脲或20 mM氯化钾的抑制。在过敏反应性收缩期间也观察到膜电位降低和动作电位的产生。作为抗原诱导的⁸⁶Rb流出变化的对照，还进行了使用高浓度氯化钾的实验。⁸⁶Rb流出根据氯化钾浓度而增加。这种增加在无钙培养基中受到抑制，但不受10 μM格列本脲的抑制。这些结果表明，在IgG介导的过敏反应性收缩期间钾离子通道的开放依赖于由于20 - 40 mM氯化钾导致的膜电位降低。所涉及的钾离子通道亚型是电压依赖性钾离子通道（Kv通道），钙激活钾离子通道（KCa通道）也可能参与⁸⁶Rb流出变化。ATP敏感性钾离子通道（KATP通道）不参与过敏反应性收缩期间钾离子通道的开放。
