Chen J G, Kempson S A
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46202-5120.
Biochim Biophys Acta. 1993 Jul 4;1149(2):299-304. doi: 10.1016/0005-2736(93)90214-k.
Deprivation of dietary phosphate leads to a decrease in urinary excretion of ammonium in rats which may be mediated through an alteration in ammonium transport in the proximal tubule. In the present study the OK renal epithelial cell line, a model for the proximal tubule, was used to determine if NH4+ transport was changed during acute phosphate deprivation. The intracellular pH after perfusion with NH4Cl solution was used for calculation of intracellular NH4+ concentration. Intracellular [NH4+] increased linearly during the first 2 min of acidification with NH4Cl. NH4+ transport, defined by the initial rate of the increase in intracellular [NH4+], was decreased by 32% (P < 0.005) in phosphate-deprived cells. This transport process was inhibited by barium chloride, but not by DIDS, amiloride or ouabain, suggesting that the NH4+ transport pathway may utilize K+ channels. Acute phosphate deprivation may inhibit NH4+ transport in OK cells by decreasing membrane K+ permeability.
饮食中缺乏磷酸盐会导致大鼠尿铵排泄减少,这可能是通过近端小管铵转运的改变介导的。在本研究中,使用OK肾上皮细胞系(一种近端小管模型)来确定急性磷酸盐缺乏期间NH4+转运是否发生变化。用NH4Cl溶液灌注后的细胞内pH用于计算细胞内NH4+浓度。在用NH4Cl酸化的前2分钟内,细胞内[NH4+]呈线性增加。由细胞内[NH4+]增加的初始速率定义的NH4+转运在磷酸盐缺乏的细胞中降低了32%(P<0.005)。该转运过程被氯化钡抑制,但不受DIDS、氨氯吡脒或哇巴因抑制,这表明NH4+转运途径可能利用K+通道。急性磷酸盐缺乏可能通过降低膜K+通透性来抑制OK细胞中的NH4+转运。