Okada Y
Membr Biochem. 1979;2(3-4):339-65. doi: 10.3109/09687687909063871.
In rat small intestine, the active transport of organic solutes results in significant depolarization of the membrane potential measured in an epithelial cell with respect to a grounded mucosal solution and in an increase in the transepithelial potential difference. According to the analysis with an equivalent circuit model for the epithelium, the changes in emf's of mucosal and serosal membranes induced by active solute transport were calculated using the measured conductive parameters. The result indicates that the mucosal cell membrane depolarizes while the serosal cell membrane remarkably hyperpolarizes on the active solute transport. Corresponding results are derived from the calculations of emf's in a variety of intestines, using the data that have hitherto been reported. The hyperpolarization of serosal membrane induced by the active solute transport might be ascribed to activation of the serosal electrogenic sodium pump. In an attempt to determine the causative factors in mucosal membrane depolarization during active solute transport, cell water contents and ion concentrations were measured. The cell water content remarkably increased and, at the same time, intracellular monovalent ion concentrations significantly decreased with glucose transport. Net gain of glucose within the cell was estimated from the restraint of osmotic balance between intracellular and extracellular fluids. In contrast to the apparent decreases in intracellular Na+ and K+ concentrations, significant gains of Na+ and K+ occurred with glucose transport. The quantitative relationships among net gains of Na+, K+ and glucose during active glucose transport suggest that the coupling ratio between glucose and Na+ entry by the carrier mechanism on the mucosal membrane is approximately 1:1 and the coupling ratio between Na+-efflux and K+-influx of the serosal electrogenic sodium pump is approximately 4:3 in rat small intestine. In addition to the electrogenic ternary complex inflow across the mucosal cell membrane, the decreases in intracellular monovalent ion concentrations, the temporary formation of an osmotic pressure gradient across the cell membrane and the streaming potential induced by water inflow through negatively charged pores of the cell membrane in the course of an active solute transport in intestinal epithelial cells are apparently all possible causes of mucosal membrane depolarization.
在大鼠小肠中，有机溶质的主动转运导致相对于接地的黏膜溶液测量的上皮细胞膜电位显著去极化，并使跨上皮电位差增加。根据上皮细胞等效电路模型的分析，利用测量的传导参数计算了主动溶质转运引起的黏膜和浆膜电动势的变化。结果表明，在主动溶质转运时，黏膜细胞膜去极化，而浆膜细胞膜显著超极化。使用迄今报道的数据，对各种肠道中的电动势进行计算也得出了相应结果。主动溶质转运引起的浆膜超极化可能归因于浆膜电生性钠泵的激活。为了确定主动溶质转运过程中黏膜膜去极化的致病因素，测量了细胞含水量和离子浓度。随着葡萄糖转运，细胞含水量显著增加，同时细胞内单价离子浓度显著降低。根据细胞内液和细胞外液之间渗透平衡的限制来估计细胞内葡萄糖的净增加量。与细胞内Na⁺和K⁺浓度的明显降低相反，葡萄糖转运时Na⁺和K⁺有显著增加。主动葡萄糖转运过程中Na⁺、K⁺和葡萄糖净增加量之间的定量关系表明，在大鼠小肠中，通过黏膜膜上载体机制的葡萄糖与Na⁺进入的偶联比约为1:1，浆膜电生性钠泵的Na⁺外流与K⁺内流的偶联比约为4:3。除了通过黏膜细胞膜的电生性三元复合物流入外，在肠道上皮细胞主动溶质转运过程中，细胞内单价离子浓度的降低、跨细胞膜渗透压梯度的暂时形成以及水通过细胞膜带负电荷的孔流入所诱导的流动电位显然都是黏膜膜去极化的可能原因。
