Jones C J, Hyde D, Lee C M, Kealey T
Q J Exp Physiol. 1986 Jan;71(1):123-32. doi: 10.1113/expphysiol.1986.sp002963.
Human eccrine sweat glands were isolated by shearing and the potential differences across the basolateral membranes determined using bevelled micro-electrodes filled with 4 M potassium acetate. Stable resting potentials of up to -81 mV were recorded. Alterations in external potassium concentration from 1.2 to 100 mM caused the membrane potential to change over a 70 mV range in cells of high resting potential, indicating that the basolateral membrane is largely potassium permeable. Input impedance was determined by constant current injection and found to be in the range 4-80 M omega. On giving a bolus injection of acetylcholine to produce a final concentration of 10(-6)-10(-7) M, four types of response were observed: depolarization, in a proportion of cells with resting potentials of -66 to -80 mV (n = 19), hyperpolarization, in a group of cells with resting potentials of -47 to -70 mV (n = 22), no change, in some cells of -40 to -81 mV resting potential (n = 22) and micro-electrode dislodgement (n = 8). In cells depolarizing to acetylcholine, the depolarization was short-lived and in thirteen cases was followed by a 'rebound' hyperpolarization. Input impedance decreased during depolarization in one-third (n = 5) of the cells in which satisfactory measurement could be made and increased during the final phase of depolarization or during rebound hyperpolarization. In cells hyperpolarizing to acetylcholine, the hyperpolarization was usually accompanied by an increase in input impedance. In ten of the twenty-two cells which showed no change to a first dose of acetylcholine, the agonist was administered at least two more times. In two cells (resting potentials -62 mV, -64 mV) a hyperpolarization was observed whereas in three others (resting potentials -66 mV, -70 mV, -81 mV) depolarization occurred. The effects of acetylcholine, whether depolarizing or hyperpolarizing, were reversibly inhibited by atropine and irreversibly reduced by ouabain. Experiments performed on glands maintained for up to 30 h in supplemented RPMI 1640 tissue culture medium yielded essentially similar results to those performed on freshly isolated glands.
通过剪切分离出人外泌汗腺,使用充满4M醋酸钾的斜角微电极测定基底外侧膜的电位差。记录到高达 -81mV的稳定静息电位。外部钾浓度从1.2mM变化到100mM时,高静息电位细胞的膜电位在70mV范围内变化,表明基底外侧膜主要对钾离子通透。通过恒流注入测定输入阻抗,发现其范围为4 - 80MΩ。给予乙酰胆碱推注以产生最终浓度为10(-6)-10(-7)M时,观察到四种类型的反应:去极化,在静息电位为 -66至 -80mV的一部分细胞中(n = 19);超极化,在静息电位为 -47至 -70mV的一组细胞中(n = 22);无变化,在一些静息电位为 -40至 -81mV的细胞中(n = 22)以及微电极移位(n = 8)。在对乙酰胆碱去极化的细胞中,去极化是短暂的,在13例中随后出现“反弹”超极化。在三分之一(n = 5)能够进行满意测量的细胞中,去极化期间输入阻抗降低,在去极化的最后阶段或反弹超极化期间增加。在对乙酰胆碱超极化的细胞中,超极化通常伴随着输入阻抗的增加。在对第一剂乙酰胆碱无变化的22个细胞中的10个细胞中,至少再给予两次激动剂。在两个细胞(静息电位 -62mV, -64mV)中观察到超极化,而在另外三个细胞(静息电位 -66mV, -70mV, -81mV)中发生去极化。乙酰胆碱的作用,无论是去极化还是超极化,均被阿托品可逆性抑制,被哇巴因不可逆性减弱。在补充有RPMI 1640组织培养基中维持长达30小时的腺体上进行的实验产生了与在新鲜分离的腺体上进行的实验基本相似的结果。