ADAPTATION OF HCO-3 AND NH+4 TRANSPORT IN RAT MTAL - EFFECTS OF CHRONIC METABOLIC-ACIDOSIS AND NA+ INTAKE

ADAPTATION OF HCO-3 AND NH+4 TRANSPORT IN RAT MTAL - EFFECTS OF CHRONIC METABOLIC-ACIDOSIS AND NA+ INTAKE
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DOI:
10.1152/ajprenal.1990.258.5.f1345
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发表时间:
1990-05-01
影响因子:
--
通讯作者:
GOOD, DW
GOOD, DW
中科院分区:
其他
文献类型:
--
作者:
GOOD, DW

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通过体外微灌注实验确定慢性代谢性酸中毒或慢性钠摄入量改变是否会引起大鼠髓质厚升肢(MTAL)中碳酸氢盐或铵转运的适应性变化。在所有实验中,在标准条件下,用25 mM碳酸氢盐在灌注液和浴液中研究MTAL。因此,运输速率的变化反映了小管细胞固有运输特性的适应性变化。慢性代谢性酸中毒(由口服NH4Cl负荷引起)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,但长期服用NaHCO3(饮用0.28 M NaHCO3水)可使碳酸氢盐吸收量增加50%,净铵吸收量增加54%。长期给盐(0.28 M NaCl饮用H2O)也增加了50%的碳酸氢盐吸收。因此,当钠与氯化物或碳酸氢盐一起服用时,钠摄入量的增加对碳酸氢盐吸收能力的刺激程度相似。适度的饮食钠限制(0.5% NaCl)与配对喂养的钠补充对照组(2.2% NaCl)相比,减少了20%的碳酸氢盐吸收。这些结果表明:1)MTAL是肾脏酸碱转运的调控位点;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,这种变化适合纠正酸中毒;3)膳食钠摄入量是MTAL碳酸氢盐和铵转运能力的重要决定因素。MTAL对钠摄入量变化的响应表明,当NaCl摄入量改变时,该部分可能在维持酸碱平衡中起重要作用。
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.