2. Experiments were performed in control rats, in animals undergoing metabolic acidosis or alkalosis and in control and acidotic rats receiving the carbonic anydrase inhibitor Diamox. 3. In all experiments, the rates of tubular bicarbonate reabsorption and of phosphate acidification (H ion secretion) were proportional to luminal buffer levels. The change of luminal acid concentrations followed first-order kinetics.4. Steady-state transepithelial pH differences were reduced in metabolic alkalosis and after diamox but augmented during metabolic acidosis.5. Acidification half-times were prolonged in metabolic acidosis and after Diamox but remained similar to control levels in metabolic alkalosis.6. From the observation that both bicarbonate reabsorption and * Supported by grants from Fundacao de Amparo a Pesquisa do Est. Sao Paulo, Cons.

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Acidification in proximal tubule of the isolated rat kidney, perfused in vitro, was studied by stopped-flow microperfusion techniques, using Sb microelectrodes to measure luminal pH. The kidney was perfused with mammalian Ringer's solution at pH 7.4 buffered by 20 mmol/l phosphate and containing 7.5 g/100 ml bovine albumin, equilibrated with air. Final urine pH was 6.88 +/- 0.5. Steady-state pH in proximal segments was 6.81 +/- 0.03 (n = 80), and acidification half-time (t/2) 7.25 +/- 0.33 (80) s, giving a net secretory H+ ion flux of 0.51 +/- 0.05 nmol . cm-2 . s-1. This flux was about 70% of "in vivo" (blood perfused kidneys). During luminal perfusion with solutions at pH 6.2, back-flux of H+ was 0.82 +/- 0.08 nmol . cm-2 . s-1, with an alkalinization t/2 of 6.33 +/- 0.34 (34) s. The difference between acidification and alkalization t/2 was not significant. This is compatible with a pump-leak system of H+ transport. This is compatible with a pump-leak system of H+ transport. The back flux of H from the lumen was markedly reduced in low Na+ perfused kidneys in the presence of 10(-4) mol/l amiloride in the lumen, indicating that this process is mediated by the luminal Na/H exchanger. Observations in the presence of high K levels suggest that it may have also a charged component. 10(-4) mol/l acetazolamide added to the kidney perfusate reduced acidification to 0.5% of control, and 10(-6) mol/l SITS to 25% of control. Thus, despite the low pCO2 (0.1-0.4 kPa, or 1-3 mm Hg), the CO2/HCO-3 buffer system still plays an important role in tubular acidification in this preparation.

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