Cellular and Molecular Mechanisms of Renal Phosphate Transport
Cellular and Molecular Mechanisms of Renal Phosphate Transport
复制标题
DOI:
10.1359/jbmr.1997.12.2.159
复制
发表时间:
1997-02
影响因子:
6.2
通讯作者:
H. Tenenhouse
中科院分区:
文献类型:
--
作者:
H. Tenenhouse
(Pi) homeostasis and, as such, plays a key role in bone mineralization and growth. The bulk of filtered Pi is reabsorbed in the proximal tubule, with approximately 60% of the filtered load reclaimed in the proximal convoluted tubule and 15‐20% in the proximal straight tubule. In addition, a small but variable portion (,10%) of filtered Pi is reabsorbed in more distal segments of the nephron. The overall capacity of the kidney to reabsorb Pi can be estimated by measuring the maximum tubular capacity (Tm) for Pi per unit volume of glomerular filtrate (TmPi/GFR). In practice, this is achieved by measuring Pi and creatinine excretions and plasma concentrations during acute Pi infusions. (1) Considerable effort has been devoted to the study of Pi transport in the proximal tubule, the principal site of its reabsorption (for reviews, see Refs. 2‐8). A wide variety of experimental systems, from the intact animal to vesicular membrane preparations, have been used to characterize proximal tubular Pi transport systems and to elucidate mechanisms involved in their regulation. These issues are briefly reviewed in the context of recent advances in the cloning of cDNAs encoding renal-specific Na 1 -Pi cotransporters and the application of these new tools to study the role of Na 1 -Pi cotransporter genes in Mendelian disorders of renal Pi reabsorption. (9‐13)