Jentsch T J, Keller S K, Wiederholt M
Curr Eye Res. 1985 Apr;4(4):361-9. doi: 10.3109/02713688509025149.
Intracellular potential measurements of confluent monolayers of cultured bovine corneal endothelial cells were used to define passive ion transport processes in these cells. Previous studies (Jentsch et al., J. Membr. Biol. 78:103 (1984); Jentsch et al., J. Membr. Biol. 81:189 (1984] have provided the experimental basis for a cellular model, in which bicarbonate entry across the basolateral membrane is indirectly driven by a Na+/H+-exchanger, which is inhibitable by amiloride (1mM). Bicarbonate and sodium should leave the cell via an electrogenic bicarbonate sodium cotransport, which is inhibitable by the disulfonic stilbene derivates SITS or DIDS. This model is also consistent with results from transendothelial studies. In this paper, we briefly review the evidence we have obtained for this model and demonstrate, that the electrical response to sodium (depolarization upon Na+-removal) is neither due to an inhibition of Na+/K+-ATPase nor explainable in terms of changes in K+-conductance. This is concluded from the observation of these responses in the presence of ouabain (10(-4)M) or barium (1mM).
利用培养的牛角膜内皮细胞汇合单层的细胞内电位测量来确定这些细胞中的被动离子转运过程。先前的研究(Jentsch等人,《膜生物学杂志》78:103 (1984);Jentsch等人,《膜生物学杂志》81:189 (1984))为一个细胞模型提供了实验依据,在该模型中,碳酸氢根跨基底外侧膜的进入是由一种钠/氢交换体间接驱动的,该交换体可被氨氯吡脒(1 mM)抑制。碳酸氢根和钠离子应通过一种生电性碳酸氢根 - 钠共转运体离开细胞,该共转运体可被二磺基芪衍生物SITS或DIDS抑制。这个模型也与跨内皮研究的结果一致。在本文中,我们简要回顾了我们为该模型获得的证据,并证明对钠的电反应(去除钠离子后去极化)既不是由于钠钾ATP酶的抑制,也不能用钾电导的变化来解释。这是通过在哇巴因(10(-4)M)或钡(1 mM)存在的情况下观察这些反应得出的结论。