Novak I, Pedersen P S, Larsen E H
Zoophysiological Laboratory A, August Krogh Institute, University of Copenhagen, Denmark.
Pflugers Arch. 1992 Nov;422(2):151-8. doi: 10.1007/BF00370414.
The purpose of this study was to characterize the ion conductances, in particular those for Cl- and K+, of human sweat duct cells grown in primary culture. Sweat duct cells from healthy individuals were grown to confluence on a dialysis membrane, which was then mounted in a mini-Ussing chamber and transepithelial and intracellular potentials were measured under open-circuit conditions. Under control conditions the epithelia developed mucosa-negative transepithelial potentials, Vte, of about -10 mV. The apical membrane potential, Va, was -25 mV to -30 mV (n = 97) in most cells, but several cells had a higher potential of about -55 mV (n = 29). Mucosal amiloride (10 mumol/l) hyperpolarized Va from -31 +/- 1 mV to a new sustained level of -46 +/- 2 mV (n = 36). These changes were accompanied by increase in the fractional resistance of the apical membrane, fRa, and decreases of Vte and the equivalent short-circuit current, Isc. In amiloride-treated tissues an increase in mucosal K+ concentration (5 mmol/l to 25 mmol/l) depolarized Va by 5 +/- 1 mV (n = 8), while the same step on the serosal side depolarized Va by 20 +/- 2 mV (n = 8). A Cl- channel blocker 3',5-dichlorodiphenylamine-2-carboxylate DCl-DPC; 10 mumol/l) depolarized Va by 5 +/- 1 mV (n = 6), an effect that was lost after amiloride application. The blocker had no effect from the serosal side. Reduction of mucosal Cl- (from 120 to 30 or 10 mmol/l) depolarized Va by 9-11 mV (n = 35), an effect that was often followed by a secondary hyperpolarization of 10-30 mV (n = 27).(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是对原代培养的人汗腺导管细胞的离子电导特性进行表征,尤其是氯离子和钾离子的电导特性。从健康个体获取的汗腺导管细胞在透析膜上生长至汇合,然后将透析膜安装在微型尤斯灌流室中,并在开路条件下测量跨上皮电位和细胞内电位。在对照条件下,上皮组织产生约 -10 mV的黏膜负跨上皮电位Vte。大多数细胞的顶端膜电位Va为 -25 mV至 -30 mV(n = 97),但有几个细胞的电位较高,约为 -55 mV(n = 29)。黏膜应用氨氯地平(10 μmol/l)使Va从 -31 ± 1 mV超极化至新的稳定水平 -46 ± 2 mV(n = 36)。这些变化伴随着顶端膜的分数电阻fRa增加,以及Vte和等效短路电流Isc降低。在氨氯地平处理的组织中,黏膜钾离子浓度从5 mmol/l增加到25 mmol/l使Va去极化5 ± 1 mV(n = 8),而在浆膜侧进行相同步骤使Va去极化20 ± 2 mV(n = 8)。氯离子通道阻滞剂3',5 - 二氯二苯胺 - 2 - 羧酸盐(DCl - DPC;10 μmol/l)使Va去极化5 ± 1 mV(n = 6),应用氨氯地平后该效应消失。该阻滞剂从浆膜侧施加无作用。黏膜氯离子浓度从120 mmol/l降至30或10 mmol/l使Va去极化9 - 11 mV(n = 35),这种效应之后常伴随10 - 30 mV的二次超极化(n = 27)。(摘要截断于250字)