Wingo C S
J Clin Invest. 1986 Nov;78(5):1324-30. doi: 10.1172/JCI112718.
The present studies examined the effect of acute in vitro acidosis on chloride reabsorption in the rabbit cortical thick ascending limb of Henle (cTALH). Four protocols were used: hypercapnic acidosis; "isocapnic" peritubular acidosis (bath bicarbonate reduction to 10 mM); isocapnic luminal acidosis (luminal bicarbonate reduction to 10 mM); isocapnic peritubular acidosis in the absence of luminal potassium. Transepithelial voltage (VT) decreased during hypercapnic acidosis and increased with recovery. Chloride reabsorption (pmol X mm-1 X min-1) decreased from 50.3 +/- 8.4 to 15.7 +/- 5.6, then increased to 45.6 +/- 11.1 with recovery. Likewise, VT was decreased reversibly during isocapnic peritubular acidosis, and chloride reabsorption decreased by 60%. Chloride reabsorption was greater (28.3 +/- 3.6) when tubules were perfused at normal luminal pH than at an acidotic luminal pH (11.4 +/- 4.5; P less than 0.05). Luminal potassium removal reduced chloride transport, and acidosis had no significant additional effect. Decreased chloride reabsorption in the cTALH during acidosis could contribute to the chloruresis associated with systemic acidosis. The symmetrical nature of this effect suggests that acidosis inhibits chloride reabsorption through an effect on cytosolic pH.
本研究检测了急性体外酸中毒对兔髓袢升支粗段（cTALH）氯重吸收的影响。采用了四种方案：高碳酸血症性酸中毒；“等碳酸血症性”肾小管周酸中毒（浴液中碳酸氢盐降至10 mM）；等碳酸血症性管腔酸中毒（管腔中碳酸氢盐降至10 mM）；无管腔钾存在时的等碳酸血症性肾小管周酸中毒。高碳酸血症性酸中毒期间跨上皮电压（VT）降低，恢复时升高。氯重吸收（pmol×mm⁻¹×min⁻¹）从50.3±8.4降至15.7±5.6，恢复时升至45.6±11.1。同样，等碳酸血症性肾小管周酸中毒期间VT可逆性降低，氯重吸收降低60%。当肾小管在正常管腔pH下灌注时氯重吸收（28.3±3.6）高于在酸性管腔pH下（11.4±4.5；P<0.05）。去除管腔钾减少了氯转运，酸中毒无显著额外影响。酸中毒期间cTALH中氯重吸收降低可能导致与全身酸中毒相关的氯尿。这种效应的对称性表明酸中毒通过对胞质pH的影响抑制氯重吸收。
