The effects of amiloride on the membrane potential of frog skeletal muscle fibres were investigated with a single intracellular microelectrode. Two microelectrode current- and voltage-clamp experiments were also performed to determine the effects of amiloride on the electrical constants and membrane current near the resting potential. 2. Amiloride reversibly hyperpolarized muscle fibres up to ca 12 mV in 2.5 mM-K+, in a concentration-dependent manner, with a half-maximum effect at 0.2 mM. Amiloride (0.4 mM) also significantly increased the membrane resistance of muscle fibres. 3. The effects of amiloride were consistent with the classical theory of the resting potential and could be described by assuming that it removes the Na+ permeability factor in the Goldman-Hodgkin-Katz equation for [K+]o > or = 2.5 mM. 4. Replacement of [Na+]o by N-methyl-glucamine, choline or Mg2+ produced smaller effects on the resting potential and on membrane resistance than those induced by amiloride. 5. It is concluded that an amiloride-sensitive poorly selective conductance continuously depolarizes the cellular membrane thus playing a role in the resting potential of frog skeletal muscle.
摘要
用单个细胞内微电极研究了氨氯地平对蛙骨骼肌纤维膜电位的影响。还进行了两个微电极电流钳和电压钳实验,以确定氨氯地平对静息电位附近电常数和膜电流的影响。2. 在2.5 mM - K⁺ 中,氨氯地平以浓度依赖性方式使肌肉纤维可逆性超极化高达约12 mV,在0.2 mM时达到最大效应的一半。氨氯地平(0.4 mM)也显著增加了肌肉纤维的膜电阻。3. 氨氯地平的作用与静息电位的经典理论一致,并且可以通过假设它在 [K⁺]o≥2.5 mM 时去除戈德曼 - 霍奇金 - Katz 方程中的 Na⁺ 通透性因子来描述。4. 用 N - 甲基葡糖胺、胆碱或 Mg²⁺ 替代 [Na⁺]o 对静息电位和膜电阻产生的影响比氨氯地平引起的影响小。5. 得出结论,氨氯地平敏感的非选择性电导持续使细胞膜去极化,从而在蛙骨骼肌的静息电位中起作用。