Cell pH (pHc) was examined by the [14C]DMO technique in suspensions of proximal tubule fragments from rabbit renal cortex. In buffer with 10 mM HCO-3, pHc was more alkaline than external pH (pHe) at values of the latter <7.4. Maximal cell-to-extracellular pH gradients (ΔpH) occurred at pHe = 6.8 and below. At pHe >7.4, pHc was more acid than pHe was. However, pHc was always more alkaline than the electrochemical equilibrium pH. At pHe ≃ 7.0, 60 min of deoxygenation decreased ΔpH from 0.22 ± 0.02 to 0.05 ± 0.01. Reoxygenation restored ΔpH to control values. Incubation with ouabain abolished the ΔpH. Both the carbonic anhydrase inhibitor, acetazolamide, and the anion transport inhibitor, 4-acetamido-4'-isothiocyano-2,2'-disulfonic stilbene (SITS), increased ΔpH. 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 HCO-3 generation with acetazolamide or blocking of HCO-3 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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Renal Fluid and Electrolyte Physiology|
|State||Published - 1980|
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