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Research Article Free access | 10.1172/JCI109570
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143
Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Department of Physiology, University of California, San Francisco, San Francisco, California 94143
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Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143
Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Department of Physiology, University of California, San Francisco, San Francisco, California 94143
Find articles by Maddox, D. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143
Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Department of Physiology, University of California, San Francisco, San Francisco, California 94143
Find articles by Lucci, M. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143
Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Department of Physiology, University of California, San Francisco, San Francisco, California 94143
Find articles by Rector, F. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143
Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Department of Physiology, University of California, San Francisco, San Francisco, California 94143
Find articles by Mueller, M. in: JCI | PubMed | Google Scholar
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, California 94143
Department of Medicine, University of California, San Francisco, San Francisco, California 94143
Department of Physiology, University of California, San Francisco, San Francisco, California 94143
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Published November 1, 1979 - More info
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 (≅1.3% body wt), single nephron glomerular filtration rate (SNGFR), and the filtered total CO2 load increased by 50%. Absolute proximal reabsorption of total CO2 (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 CO2 reabsorption decreased from 0.90 to 0.77. Aortic constriction in these plasma-repleted rats returned the filtered load and reabsorption of total CO2 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 CO2 reabsorption (0.76-0.81).
Metabolic acidosis was associated with very high fractional proximal total CO2 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 CO2 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 CO2 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.