Ussing H H
Acta Physiol Scand. 1982 Mar;114(3):363-9. doi: 10.1111/j.1748-1716.1982.tb06996.x.
Previous results (MacRobbie & Ussing 1961) in combination with published values for cellular chloride concentration and for intracellular potentials show that the chloride concentration in frog skin epithelium cells is higher than predicted for equilibrium with the inside bathing solution. Both the apical and the basolateral membrane of these cells are normally almost tight to chloride, so that the maintenance of the high chloride concentration requires little work. A basolateral permeability to chloride is, however, activated by cell swelling, and the cells lose KCl. It is now shown that the KCl thus lost cannot be regained neither in the absence of sodium in the inside bath nor in the presence of furosemide. The volume regulation reactions are, however, independent of the composition of the outside bath. It is concluded that the recovery of KCl by the epithelium is due to a basolateral co-transport of NaCl from medium to cells, combined with return of Na to the medium via the Na-K pump. The co-transport mechanism thus restores the high chloride concentration of the cells, but seems to be virtually dormant unless the cells have lost chloride.
先前的研究结果(MacRobbie和Ussing,1961年)与已发表的细胞内氯离子浓度及细胞内电位值相结合表明,蛙皮上皮细胞中的氯离子浓度高于根据与内部浸泡溶液达到平衡所预测的浓度。这些细胞的顶端膜和基底外侧膜通常对氯离子几乎是紧密的,因此维持高氯离子浓度所需的工作量很小。然而,细胞肿胀会激活基底外侧对氯离子的通透性,细胞会失去氯化钾。现在表明,无论是在内部浴液中没有钠的情况下,还是在存在呋塞米的情况下,失去的氯化钾都无法重新获得。然而,体积调节反应与外部浴液的成分无关。得出的结论是,上皮细胞对氯化钾的恢复是由于基底外侧将氯化钠从中介质共转运到细胞中,并通过钠钾泵将钠返回介质。因此,共转运机制恢复了细胞的高氯离子浓度,但除非细胞失去了氯离子,否则该机制似乎实际上处于休眠状态。