Good D W
Department of Physiology, University of Texas Medical Branch, Galveston 77550.
Am J Physiol. 1990 May;258(5 Pt 2):F1345-53. doi: 10.1152/ajprenal.1990.258.5.F1345.
In vitro microperfusion experiments were performed to determine whether chronic metabolic acidosis or chronic alterations in sodium intake cause adaptive changes in bicarbonate or ammonium transport in the medullary thick ascending limb (MTAL) of the rat. In all experiments, MTAL were studied under standard conditions in vitro with 25 mM bicarbonate in perfusate and bath. Thus changes in transport rates reflect adaptive changes in the intrinsic transport properties of the tubule cells. Chronic metabolic acidosis (induced by oral NH4Cl loading) increased MTAL bicarbonate absorption by 53% and increased net ammonium absorption by 36%. Chronic administration of NaHCO3 (0.28 M NaHCO3 drinking H2O) increased MTAL bicarbonate absorption by 50% and increased net ammonium absorption by 54%, despite systemic metabolic alkalosis. Chronic administration of NaCl (0.28 M NaCl drinking H2O) also increased bicarbonate absorption by 50%. Thus an increase in sodium intake stimulated bicarbonate absorptive capacity to a similar extent when sodium was administered with either chloride or bicarbonate. Moderate dietary sodium restriction (0.5% NaCl) reduced bicarbonate absorption by 20% compared with pair-fed sodium-replete controls (2.2% NaCl). These results demonstrate that 1) the MTAL is a site of regulation of renal acid-base transport, 2) chronic metabolic acidosis is associated with adaptive increases in MTAL bicarbonate and ammonium absorption, changes that are appropriate to correct the acidosis, and 3) dietary sodium intake is an important determinant of MTAL bicarbonate and ammonium transport capacity. The response of the MTAL to changes in sodium intake suggests that this segment may play an important role in maintaining acid-base balance when NaCl intake is altered.
进行体外微灌注实验，以确定慢性代谢性酸中毒或钠摄入量的慢性改变是否会引起大鼠髓袢升支粗段（MTAL）中碳酸氢盐或铵转运的适应性变化。在所有实验中，MTAL在体外标准条件下进行研究，灌注液和浴液中含有25 mM碳酸氢盐。因此，转运速率的变化反映了肾小管细胞内在转运特性的适应性变化。慢性代谢性酸中毒（通过口服氯化铵负荷诱导）使MTAL碳酸氢盐吸收增加53%，净铵吸收增加36%。尽管存在全身性代谢性碱中毒，但慢性给予NaHCO₃（0.28 M NaHCO₃饮用H₂O）使MTAL碳酸氢盐吸收增加50%，净铵吸收增加54%。慢性给予NaCl（0.28 M NaCl饮用H₂O）也使碳酸氢盐吸收增加50%。因此，当钠与氯或碳酸氢盐一起给予时，钠摄入量的增加会在相似程度上刺激碳酸氢盐吸收能力。与成对喂养的钠充足对照组（2.2% NaCl）相比，适度的饮食钠限制（0.5% NaCl）使碳酸氢盐吸收减少20%。这些结果表明：1）MTAL是肾酸碱转运的调节部位；2）慢性代谢性酸中毒与MTAL碳酸氢盐和铵吸收的适应性增加有关，这些变化有助于纠正酸中毒；3）饮食钠摄入量是MTAL碳酸氢盐和铵转运能力的重要决定因素。MTAL对钠摄入量变化的反应表明，当NaCl摄入量改变时，该节段可能在维持酸碱平衡中起重要作用。
