Kondo Y, Frömter E
Zentrum der Physiologie, Johann-Wolfgang-Goethe-Universität, Frankfurt, Federal Republic of Germany.
Pflugers Arch. 1990 Mar;415(6):726-33. doi: 10.1007/BF02584012.
The mechanism of HCO3- exit from rabbit renal proximal tubule S3 segments was investigated. Isolated tubules were perfused luminally and peritubularly with test solutions and cell pH (pHi), cell Cl- activity ([Cl-]i) and cell Na+ activity ([Na+]i) were measured with ion-selective microelectrodes. From the response of pHi and [Cl-]i to changes in bath Cl- or HCO3- concentrations a Cl-/HCO3- exchanger was identified in the basolateral cell membrane. It was reversibly inhibited by millimolar concentrations of the disulfonic stilbene SITS (4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid). Cell potential measurements and preliminary determinations of initial ion flux rates suggested a stoichiometry of Cl- to HCO3- flux near 1.0. The transport rate appeared to saturate already at low bath Cl- concentrations (approximately 30 mmol/l), but it was independent of bath pH in the range of 7.4-6.4. Cl-/HCO3- exchange was not directly coupled to Na+ flux although in approximately half of the experiments long-term incubation in Na(+)-free solutions indirectly inhibited the exchanger. Sudden application of SITS under control conditions revealed that the exchanger normally facilitates the exit of HCO3- from cell to interstitium at the expense of Cl- uptake into the cell. How Cl- ions recirculate towards the peritubular surface is presently not known.
研究了兔肾近端小管S3段中HCO₃⁻排出的机制。用测试溶液对分离出的小管进行管腔和管周灌注，并用离子选择性微电极测量细胞内pH（pHi）、细胞内Cl⁻活性（[Cl⁻]i）和细胞内Na⁺活性（[Na⁺]i）。根据pHi和[Cl⁻]i对浴液中Cl⁻或HCO₃⁻浓度变化的反应，在基底外侧细胞膜中鉴定出一种Cl⁻/HCO₃⁻交换体。它被毫摩尔浓度的二磺酸芪SITS（4-乙酰氨基-4'-异硫氰酸芪-2,2'-二磺酸）可逆性抑制。细胞电位测量和初始离子通量率的初步测定表明，Cl⁻与HCO₃⁻通量的化学计量比接近1.0。转运速率在低浴液Cl⁻浓度（约30 mmol/l）时似乎就已饱和，但在7.4 - 6.4的pH范围内与浴液pH无关。Cl⁻/HCO₃⁻交换并不直接与Na⁺通量偶联，尽管在大约一半的实验中，在无Na⁺溶液中长期孵育会间接抑制该交换体。在对照条件下突然应用SITS表明，该交换体通常促进HCO₃⁻从细胞排出到间质，代价是Cl⁻摄入细胞。目前尚不清楚Cl⁻离子如何向管周表面再循环。
