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正常和酸中毒大鼠近端碳酸氢盐重吸收的调控

Control of proximal bicarbonate reabsorption in normal and acidotic rats.

作者信息

Cogan M G, Maddox D A, Lucci M S, Rector F C

出版信息

J Clin Invest. 1979 Nov;64(5):1168-80. doi: 10.1172/JCI109570.

Abstract

This free-flow micropuncture study examined the dependence of bicarbonate reabsorption in the rat superficial proximal convoluted tubule to changes in filtered bicarbonate load, and thereby the contribution of the proximal tubule to the whole kidney's response to such changes. The independent effects of extracellular fluid (ECF) volume expansion and of acidosis on proximal bicarbonate reabsorption were also examined. When the plasma volume contraction incurred by the micropuncture preparatory surgery was corrected by isoncotic plasma infusion ( congruent with1.3% body wt), single nephron glomerular filtration rate (SNGFR), and the filtered total CO(2) load increased by 50%. Absolute proximal reabsorption of total CO(2) (measured by microcalorimetry) increased by 30%, from 808+/-47 during volume contraction to 1,081+/-57 pmol/min.g kidney wt after plasma repletion, as fractional total CO(2) reabsorption decreased from 0.90 to 0.77. Aortic constriction in these plasma-repleted rats returned the filtered load and reabsorption of total CO(2) to the previous volume contracted levels. In other animals isohydric ECF expansion with plasma (5% body wt) or Ringer's solution (10% body wt), or both, produced no further diminution in fractional proximal total CO(2) reabsorption (0.76-0.81). Metabolic acidosis was associated with very high fractional proximal total CO(2) reabsorptive rates of 0.82 to 0.91 over a wide range of SNGFR and ECF volumes. At a single level of SNGFR, end-proximal total CO(2) concentration progressively decreased from 5.6+/-0.5 to 1.6 +/-0.2 mM as arterial pH fell from 7.4 to 7.1. Expansion of ECF volume in the acidotic rats did not inhibit the ability of the proximal tubule to lower end-proximal total CO(2) concentrations to minimal levels. In conclusion, bicarbonate reabsorption in the superficial proximal convoluted tubule is highly load-dependent (75-90%) in normal and acidotic rats. No inhibitory effect of ECF volume per se on proximal bicarbonate reabsorption, independent of altering the filtered bicarbonate load, could be discerned. Acidosis enabled the end-proximal luminal bicarbonate concentration to fall below normal values and reduced distal bicarbonate delivery.

摘要

这项自由流动微穿刺研究检测了大鼠浅表近端曲管中碳酸氢盐重吸收对滤过碳酸氢盐负荷变化的依赖性,进而检测了近端小管对全肾对此类变化反应的贡献。还检测了细胞外液(ECF)容量扩张和酸中毒对近端碳酸氢盐重吸收的独立影响。当通过输注等渗血浆(相当于体重的1.3%)纠正微穿刺准备手术引起的血浆容量收缩时,单肾单位肾小球滤过率(SNGFR)和滤过的总CO₂负荷增加了50%。总CO₂的绝对近端重吸收(通过微量热法测量)增加了30%,从容量收缩期间的808±47增加到血浆补充后的1081±57 pmol/min·g肾重,而总CO₂重吸收分数从0.90降至0.77。在这些血浆补充后的大鼠中进行主动脉缩窄,使滤过负荷和总CO₂重吸收恢复到先前容量收缩水平。在其他动物中,用血浆(体重的5%)或林格氏液(体重的10%)或两者进行等渗ECF扩张,不会使近端总CO₂重吸收分数进一步降低(0.76 - 0.81)。在广泛的SNGFR和ECF容量范围内,代谢性酸中毒与非常高的近端总CO₂重吸收率(0.82至0.91)相关。在单一SNGFR水平,随着动脉pH从7.4降至7.1,近端末端总CO₂浓度从5.6±0.5逐渐降至1.6±0.2 mM。在酸中毒大鼠中扩张ECF容量并未抑制近端小管将近端末端总CO₂浓度降至最低水平的能力。总之,在正常和酸中毒大鼠中,浅表近端曲管中的碳酸氢盐重吸收高度依赖负荷(75 - 90%)。未发现ECF容量本身对近端碳酸氢盐重吸收有独立于改变滤过碳酸氢盐负荷的抑制作用。酸中毒使近端末端管腔碳酸氢盐浓度降至正常值以下,并减少了远端碳酸氢盐的输送。

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