Münich G, Dietl P, Oberleithner H
Pflugers Arch. 1986;407 Suppl 2:S60-5. doi: 10.1007/BF00584931.
The hypothesis was tested whether amiloride and/or an acute acid load influence Cl- transport in the diluting segment of the isolated-perfused kidney of the K+ adapted frog (rana pipiens). Transepithelial resistance (luminal cable analysis) and Cl- net flux (Cl- sensitive microelectrodes) were evaluated at various concentrations of amiloride, at high pCO2 or low HCO-3 in the kidney perfusate. Amiloride or an acute acid load increase transepithelial resistance. The resistance-change at given concentrations of amiloride is markedly enhanced under static head conditions, i.e. at low luminal NaCl concentrations. Amiloride or acidosis (high pCO2) reduce Cl- net reabsorption; combination of both potentiates this inhibitory effect. We conclude: an acute acid load acidifies the cell cytosol. This effect is aggravated dramatically after amiloride-induced inhibition of the luminal Na+/H+ exchanger. The luminal pH-sensitive K+ conductance decreases. This results in a depolarization of the cell membranes. Consequently, the peritubular electrochemical driving force for the exit step of Cl- (from cell to blood) dissipates. Therefore, Cl- net reabsorption is blunted.
研究了氨氯吡咪和/或急性酸负荷是否会影响适应钾的青蛙(牛蛙)离体灌注肾脏稀释段中的氯离子转运。在不同浓度的氨氯吡咪、肾脏灌注液中高二氧化碳分压或低碳酸氢根浓度条件下,评估跨上皮电阻(管腔电缆分析)和氯离子净通量(氯离子敏感微电极)。氨氯吡咪或急性酸负荷会增加跨上皮电阻。在静态水头条件下,即在低管腔氯化钠浓度时,给定浓度氨氯吡咪引起的电阻变化会显著增强。氨氯吡咪或酸中毒(高二氧化碳分压)会降低氯离子的净重吸收;两者联合使用会增强这种抑制作用。我们得出结论:急性酸负荷会使细胞胞质酸化。在氨氯吡咪诱导抑制管腔钠/氢交换体后,这种效应会显著加剧。管腔pH敏感钾电导降低。这导致细胞膜去极化。因此,氯离子从细胞排出到血液的肾小管周围电化学驱动力消失。所以,氯离子的净重吸收受到抑制。