Murer H, Lötscher M, Kaissling B, Levi M, Kempson S A, Biber J
Institute of Physiology, University of Zürich, Switzerland.
Kidney Int. 1996 Jun;49(6):1769-73. doi: 10.1038/ki.1996.264.
Inorganic phosphate (Pi) is reabsorbed in renal proximal tubules in a sodium (Na)-dependent manner involving brush border Na/Pi-cotransporter(s). Regulation of renal Pi-reabsorption, such as by parathyroid hormone (PTH) and/or by dietary Pi-deprivation, involves alterations in the rate of Na/Pi-cotransport. Two structurally different Na/Pi-cotransporters have been identified: type I-transporter and type II-transporter. The related mRNAs and proteins are located in the proximal tubule and in the brush border membrane. In heterologous expression systems type I and type II Na/Pi-cotransporters mediate Na/Pi-cotransport. Characterization of the transport properties suggested that the type II transporter is "responsible' for brush border membrane Na/Pi-cotransport (as observed in isolated vesicles). Administration of PTH to rats resulted in an inhibition of brush border membrane Na/Pi-cotransport (vesicles) and in a reduced brush border membrane content of the type II transporter. Feeding low Pi-diets resulted in an up-regulation of Na/Pi-cotransport (vesicles) and of type II transporter content; only after a prolonged exposure to low Pi-diets (more than 4 hr) was an increase in specific mRNA content observed. Refeeding high Pi diets had the opposite effects on Na/Pi-cotransport activity and on type II transporter protein. It is currently the task of future experiments to define the specific mechanisms leading to protein-synthesis-independent (PTH, acute Pi-deprivation, Pi-refeeding) and to protein-synthesis-dependent (prolonged Pi-deprivation) regulation of the type II Na/Pi-cotransporter.
无机磷酸盐（Pi）以依赖钠（Na）的方式在肾近端小管中被重吸收，这涉及刷状缘钠/磷酸盐共转运体。肾Pi重吸收的调节，如通过甲状旁腺激素（PTH）和/或通过饮食中Pi缺乏，涉及钠/磷酸盐共转运速率的改变。已鉴定出两种结构不同的钠/磷酸盐共转运体：I型转运体和II型转运体。相关的mRNA和蛋白质位于近端小管和刷状缘膜中。在异源表达系统中，I型和II型钠/磷酸盐共转运体介导钠/磷酸盐共转运。转运特性的表征表明，II型转运体“负责”刷状缘膜钠/磷酸盐共转运（如在分离的囊泡中观察到的）。给大鼠注射PTH导致刷状缘膜钠/磷酸盐共转运（囊泡）受到抑制，并且II型转运体的刷状缘膜含量降低。喂食低Pi饮食导致钠/磷酸盐共转运（囊泡）和II型转运体含量上调；仅在长期暴露于低Pi饮食（超过4小时）后，才观察到特定mRNA含量增加。重新喂食高Pi饮食对钠/磷酸盐共转运活性和II型转运体蛋白具有相反的影响。确定导致II型钠/磷酸盐共转运体蛋白质合成非依赖性（PTH、急性Pi缺乏、Pi再喂食）和蛋白质合成依赖性（长期Pi缺乏）调节的具体机制是未来实验的任务。
