The Mechanism of Bicarbonate Reabsorption in the Proximal and Distal Tubules of the Kidney.


Considerable evidence (1-6) has been adduced to support the hypothesis that the reabsorption of filtered HCO3by the kidney is mediated by a single mechanism, operative in both the proximal and distal portions of the nephron, which involves the secretion of cellular He in exchange for luminal Na+. The secreted Ho reacts with filtered HC03to form H2CO3, which then decomposes to C02 and H20. Difficulties arise, however, when the details of the process are examined. In the steady state, the rate at which the H2CO3 is removed from the luminal fluid must equal the rate at which H+ is secreted. Walser and Mudge (7) have estimated that for the uncatalyzed dehydration of H2C03 to account for the observed rates of HC03reabsorption, the steady-state concentration of H2C03 in luminal fluid must be at least tenfold greater than the concentration that would exist were H2C03 in equilibrium with the C02 tension of luminal fluid and plasma. As a result of the excess H2C03, the steady-state pH would be approximately 1 pH U lower than would be predicted from the luminal concentration of HC03and the C02 tension of plasma, assuming complete equilibration of luminal H2C03 with plasma C02. A marked disequilibrium pH ' would exist. Two lines of evidence have been advanced to support the presence of a disequilibrium pH in the proximal tubule. Rector and Carter (8) perfused single proximal tubules with NaHCO3

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@article{Rector1965TheMO, title={The Mechanism of Bicarbonate Reabsorption in the Proximal and Distal Tubules of the Kidney.}, author={Floyd C. Rector and Norman W . Carter and Donald Wayne Seldin}, journal={The Journal of clinical investigation}, year={1965}, volume={44}, pages={278-90} }