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Am J Physiol Renal Physiol 256: F751-F765, 1989;
0363-6127/89 $5.00
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AJP - Renal Physiology, Vol 256, Issue 5 751-F765, Copyright © 1989 by American Physiological Society

ARTICLES

Basolateral membrane H-OH-HCO3 transport in the proximal tubule

P. A. Preisig and R. J. Alpern
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 77235-8856.

This review focuses on the basolateral membrane mechanisms of H-OH-HCO3 transport in the proximal tubule. The mechanism that has the greatest transport capacity and mediates most of transepithelial H-HCO3 transport is the electrogenic, Na-3HCO3 cotransporter. This transporter has been extensively characterized in the salamander, rat, and rabbit proximal tubule, and has now been found in a number of other epithelia that effect transepithelial NaHCO3 transport. Transporter rate is sensitive to intra- and extracellular [Na], intra- and extracellular [HCO3]/pH, and cell voltage. Adaptations in transporter activity have been demonstrated in chronic metabolic acidosis and alkalosis, chronic respiratory acidosis and alkalosis, and chronic hyperfiltration. In addition to the Na-3HCO3 cotransporter, the basolateral membrane possesses both Na-dependent and -independent Cl-HCO3 exchangers, a H leak, and in the S3 proximal tubule an Na-H antiporter. The role of these H-OH-HCO3 transport mechanisms in transcellular HCO3 and Cl absorption and pHi defense is discussed.


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