Beck F X, Schramm M, Dörge A, Rick R, Thurau K
Physiologisches Institut, Universität München, Federal Republic of Germany.
Pflugers Arch. 1988 Sep;412(4):427-33. doi: 10.1007/BF01907563.
We studied the effect of acute metabolic acidosis on potassium, sodium and chloride gradients across the apical membrane of proximal and distal tubule cells by determining electrolyte concentrations in individual cells and in tubule fluid employing electron microprobe analysis. Cellular measurements were performed on freeze-dried cryosections of the renal cortex, analysis of tubule fluid electrolyte concentrations on freeze-dried microdroplets of micropuncture samples obtained from proximal and from early and late distal collection sites. Acidosis (NH4Cl i.v. and i.g.) induced a substantial rise in plasma potassium concentration without significant effects on cell potassium concentrations. Potassium concentrations along the surface distal tubule were also unaltered; thus the chemical driving force for potassium exit from cell to lumen was not affected by acidosis. In all but intercalated cells acidosis markedly increased cell phosphorus concentration and cell dry weight indicating cell shrinkage and thus diminution of cell potassium content. Because the increase in intracellular chloride concentration exceeded the increase in plasma chloride concentration, the chemical chloride gradient across the contraluminal membrane was markedly depressed by acidosis.
我们通过使用电子微探针分析来测定单个细胞和小管液中的电解质浓度，研究了急性代谢性酸中毒对近端和远端小管细胞顶端膜上钾、钠和氯梯度的影响。细胞测量是在肾皮质的冻干冷冻切片上进行的，小管液电解质浓度分析是在从近端以及远端早期和晚期收集部位获得的微穿刺样本的冻干微滴上进行的。酸中毒（静脉注射和口服氯化铵）导致血浆钾浓度大幅升高，但对细胞钾浓度没有显著影响。远端小管表面的钾浓度也未改变；因此，钾从细胞排出到管腔的化学驱动力不受酸中毒影响。除闰细胞外，在所有细胞中，酸中毒均显著增加了细胞磷浓度和细胞干重，表明细胞萎缩，从而细胞钾含量减少。由于细胞内氯浓度的增加超过了血浆氯浓度的增加，酸中毒显著降低了跨对腔膜的化学氯梯度。
