Mechansims and components of renal tubular acidification.
1. Renal cortical tubules of control and acetazolamide infused rats were perfused with 100 mM phosphate buffer at pH 5-5. The rate of alkalinization was measured by means of antimony micro-electrodes and was used to compute passive H ion fluxes from lumen to blood across the proximal and distal tubular epithelium. 2. The importance of other ionic movements that might contribute to pH changes of luminal buffers (chloride inflow into the lumen and bicarbonate diffusion across the epithelium) was assessed but found to be minor. H ion movements accounted for the majority of the observed pH changes. 3. H ion permeability of the tubular wall was calculated from the measured H fluxes and transepithelial concentration differences. It was 1-10 cm/sec, several orders of magnitude larger than those for other ions. However, such values are compatible with the mobility of protons in a medium of structure water within the limiting membrane. 4. A kinetic analysis of the mechanism of movement of H ions across the renal tubule is presented on the basis of experiments in which acidification and alkalinization of luminal buffers was followed in stationary microperfusions. The data are compatible with a pump-leak system in the proximal tubule, and with a model with low H ion permeability and a gradient dependent pump in the distal tubule.
D000136:Acid-Base Equilibrium; D000818:Animals; D001639:Bicarbonates / Q000378:metabolism; D001693:Biological Transport, Active; D002712:Chlorides / Q000378:metabolism; D004848:Epithelium / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007684:Kidney Tubules / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D010539:Permeability; D051381:Rats
D001639:Bicarbonates; D002712:Chlorides