Mechanism of bicarbonate exit across basolateral membrane of the rabbit proximal convoluted tubule.
To clarify the mechanism(s) of HCO-3 movement across the basolateral membrane, rabbit proximal convoluted tubules were perfused in vitro. Two possible mechanisms were examined: neutral HCO-3 exit coupled to chloride and rheogenic HCO-3 exit. A complete C1- substitution with isethionate in the lumen and bath did not affect HCO-3 reabsorption, suggesting that HCO-3 exit is not coupled to chloride. Addition of 2 mM Ba2+ to the bath, which has been shown to depolarize the basolateral membrane potential difference, caused a 42% inhibition of HCO-3 reabsorption and a 32% inhibition of volume flux, suggesting that HCO-3 exit is rheogenic. Ba2+ did not affect the volume flux when HCO-3 reabsorption was inhibited by acetazolamide, suggesting that the Ba2+ effect is not due to a general inhibition of cell metabolism. From these data we propose that HCO-3 exits the basolateral membrane by a rheogenic, chloride-independent mechanism.
D000818:Animals; D001464:Barium / Q000494:pharmacology; D001639:Bicarbonates / Q000378:metabolism*; D001692:Biological Transport; D002462:Cell Membrane / Q000502:physiology; D002712:Chlorides / Q000494:pharmacology; D004848:Epithelium / Q000502:physiology; D005260:Female; D005942:Gluconates / Q000494:pharmacology; D066298:In Vitro Techniques; D007513:Isethionic Acid / Q000494:pharmacology; D007687:Kidney Tubules, Proximal / Q000187:drug effects / Q000502:physiology*; D007700:Kinetics; D011817:Rabbits
D001639:Bicarbonates; D002712:Chlorides; D005942:Gluconates; D001464:Barium; D007513:Isethionic Acid; C030691:gluconic acid