Cell pH and acid transport in renal cortical tissue

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Abstract
Cell pH (pHc) was examined by the [14C]DMO technique in suspensions of proximal tubule fragments from rabit renal cortex. In buffer with 10 mM HCO3-, pHc was more alkaline than external pH (pHe) at values of the latter < 7.4. Maximal cell-to-extracellular pH gradients (.DELTA.pH) occurred at pHe = 6.8 and below. At pHe > 7.4, pHc was more acid than pHe was. pHc was always more alkaline than the electrochemical equilibrium pH. At pHe .simeq. 7.0, 60 min of deoxygenation decreased .DELTA.pH from 0.22 .+-. 0.02-0.05 .+-. 0.01. Reoxygenation restored .DELTA.pH to control values. Incubation with ouabain abolished the .DELTA.pH. The carbonic anhydrase inhibitor, acetazolamide, and the anion transport inhibitor, 4-acetamido-4''-isothiocyano-2,2''-disulfonic stilbene (SITS), increased .DELTA.pH. The studies demonstrate relative intracellular alkalinity in proximal tubule. A fall in pHc occurs with maneuvers that interfere with H+ pumping out of the cells. A rise in pHc occurs with maneuvers that interfere with the disposition of intracellular alkali: slowing of HCO3- generation with acetazolamide or blocking of HCO3- exit with SITS. The results support a H+-secretory model of proximal tubule acid transport that is dependent on maintenance and dispersal of intracellular alkalinity.