Okada Y, Tsuchiya W, Irimajiri A, Inouye A
J Membr Biol. 1977 Mar 8;31(3):205-19. doi: 10.1007/BF01869405.
Addition of D-glucose to the mucosal fluid resulted in a significant depolarization of the mucosal membrane potential (V-m) in rat duodenum, jejunum, and ileum accompanied by an increase in the transepithelial potential difference (PDt). On the other hand, L-glucose did not induce PDt and Vm changes. Glycine applied from the mucosal side also induced Vm-depolarization and PDt-increment in the ileum. Phlorizin added to the mucosal fluid or ouabain added to the serosal fluid inhibited the sugar-dependent changes in PDt and Vm. According to the analysis with an equivalent circuit model for the epithelium, it was concluded that an actively transported solute induced not only a depolarization of the mucosal (brush border) membrane but also a hyperpolarization of the serosal (baso-lateral) membrane of an epithelial cell, so that the origin of solute-induced PDt changes should be attributed to changes in emf's at both membranes. The hyperpolarization of the serosal membrane in the presence of an actively transported solute was attributed to a mechanism of serosal electrogenic sodium pump stimulated by the increase in the extrusion rate of Na+ co-transported into the cell with sugar or amino acid.
向黏膜液中添加D-葡萄糖会导致大鼠十二指肠、空肠和回肠的黏膜膜电位(V-m)显著去极化,同时跨上皮电位差(PDt)增加。另一方面,L-葡萄糖不会引起PDt和Vm的变化。从黏膜侧施加甘氨酸也会导致回肠Vm去极化和PDt增加。添加到黏膜液中的根皮苷或添加到浆膜液中的哇巴因会抑制PDt和Vm的糖依赖性变化。根据上皮细胞等效电路模型的分析,得出的结论是,主动转运的溶质不仅会引起上皮细胞黏膜(刷状缘)膜的去极化,还会引起浆膜(基底外侧)膜的超极化,因此溶质诱导的PDt变化的起源应归因于两个膜上电动势的变化。在存在主动转运溶质的情况下,浆膜膜的超极化归因于浆膜电生性钠泵的一种机制,该机制由与糖或氨基酸共转运进入细胞的Na+的挤出速率增加所刺激。