Moran A
Am J Physiol. 1987 Jan;252(1 Pt 1):C63-7. doi: 10.1152/ajpcell.1987.252.1.C63.
Sodium influx into LLC-PK1 cells has been characterized. The main amiloride-sensitive pathway for sodium entry through the apical membrane in this cell line is sodium-hydrogen exchange with an apparent Km for sodium of 19 mM. Influx is pH dependent and is amiloride sensitive with K1/2 of 30 microM. Inhibition of the sodium transport by protons (at 1 mM external sodium) is consistent with an interaction of H+ ions at a single site having an apparent pKH of 7.2. These data are similar to those reported previously for brush border membrane (BBM) isolated from kidney proximal tubule. However, in contrast to previously published reports, H+ does not compete with amiloride in blocking Na+ influx and exhibits a mixed inhibition with sodium ions. The latter, together with a direct and independent assessment of amiloride and sodium interaction, indicates that amiloride does not compete with sodium for the same site. Possible explanations for the discrepancy in the literature concerning the interaction of Na+, H+, and amiloride with the Na+-H+ exchanger and the characteristics of the Na+-H+ exchange system in LLC-PK1 are discussed.
已对LLC-PK1细胞中的钠内流进行了表征。在该细胞系中,通过顶端膜进入细胞的主要氨氯地平敏感途径是钠-氢交换,钠的表观Km为19 mM。内流依赖于pH,对氨氯地平敏感,K1/2为30 μM。质子对钠转运的抑制作用(在外部钠浓度为1 mM时)与H+离子在单个位点的相互作用一致,表观pKH为7.2。这些数据与先前报道的从肾近端小管分离的刷状缘膜(BBM)的数据相似。然而,与先前发表的报告不同,H+在阻断Na+内流时不与氨氯地平竞争,并且与钠离子表现出混合抑制作用。后者与对氨氯地平和钠相互作用的直接独立评估一起表明,氨氯地平不与钠竞争同一位点。讨论了关于Na+、H+和氨氯地平与Na+-H+交换体相互作用以及LLC-PK1中Na+-H+交换系统特性的文献差异的可能解释。