The role of proton trnsport in proximal tubule cells in Dent's disease.

有文献报道，肾结石的发生与Cl-通道ClC-5功能障碍有关.我们最近发现，ClC-5存在于近端和远端小管细胞在牛蛙，产生草酸钙结石在肾脏。因此，本实验旨在阐明牛蛙肾小管细胞Cl-转运变化与H+或Ca ~（2+）转运变化之间的关系。用Cl-转运抑制剂或低Cl-溶液灌流肾小管周，总是引起近端小管胞浆和小管液pH值（pHTF）或远端小管pHTF的变化。当pHTF增加时，近端和远端小管中小管液中的Ca 2+浓度（[Ca]TF）总是降低，表明[Ca]TF受pHTF调节，以对抗尿中钙盐（结石）的沉积。 因此，ClC-5功能障碍引起的Dent病可能是由H+跨小管细胞转运的变化引起的。

It has been reported that dysfunction of ClC-5, Cl- channel, produced the kidney stone. We recently demonstrated that ClC-5 existed in both the proximal and distal tubule cells in the bullfrog, producing the calcium oxalic calculus in the kidney. Therefore, in this experiment, we purposed to clarify the relationship between the changes in Cl- transport and those in H+ or Ca2+ transport in the bullfrog tubule cells. The peritubular perfusion with the inhibitor of Cl- transport, or with low Cl- solution always produced the change in pH in both cytosolic and tubular fluid (pHTF) in proximal tubule or the pHTF in the distal tubule. When the pHTF increases, Ca2+ concentration in tubular fluids ([Ca]TF) always decreases in both proximal and distal tubules, indicating that [Ca]TF is regulated by pHTF against the sedimentation of calcium salt (calculus) in the urine. Thus, Dent's disease caused by dysfunction of ClC-5 might be induced by the change in H+ transport across the tubule cells.