Biber J, Murer H
Am J Physiol. 1985 Nov;249(5 Pt 1):C430-4. doi: 10.1152/ajpcell.1985.249.5.C430.
A short-term regulation of the Na-dependent transport of Pi in LLC-PK1 cells by the extracellular concentration of Pi is described. Pi deprivation of the cells for 10 min led to an increase (30%) of the Na-Pi cotransport activity, whereas the Na-dependent D-glucose transport system was not affected. This regulatory phenomenon was not affected by the presence of cycloheximide. The same adaptive response was observed in apical membrane vesicles isolated from rapidly adapted cells. In the isolated membranes, increased Na-Pi cotransport is characterized by an increase of the maximal rate of uptake (control: 193 +/- 15; adapted: 306 +/- 51 pmol X mg-1 X 15 s-1), whereas the apparent Km for Pi remained constant. The results suggest that LLC-PK1 cells possess a mechanism or mechanisms that allow a rapid "activation" and "inactivation" of Na-dependent Pi transport systems as a function of the concentration of the extracellular Pi.
本文描述了 LLC-PK1 细胞中，细胞外无机磷（Pi）浓度对依赖钠的 Pi 转运的短期调节作用。细胞缺磷 10 分钟会导致钠-磷共转运活性增加（30%），而依赖钠的 D-葡萄糖转运系统不受影响。这种调节现象不受放线菌酮的影响。从快速适应的细胞中分离出的顶端膜囊泡也观察到了相同的适应性反应。在分离出的膜中，钠-磷共转运增加的特征是摄取最大速率的增加（对照：193±15；适应：306±51 pmol·mg⁻¹·15 s⁻¹），而 Pi 的表观 Km 保持不变。结果表明，LLC-PK1 细胞具有一种机制或多种机制，可根据细胞外 Pi 的浓度对依赖钠的 Pi 转运系统进行快速“激活”和“失活”。
