Transient renal tubular acidosis may complicate acute renal failure (ARF). To clarify this phenomenon, the present study examined tubular H+ ion secretory capacity in an ischemic model of ARF. Clearance studies were performed in dogs subjected to 60 minutes, unilateral renal artery clamping. The contralateral kidney served as control. One hour after release of clamp, mean glomerular filtration rate (GFR) was reduced by 50 to 70 percent in the ischemic kidney. Bicarbonate reclamation (mEq/liter GFR) was comparable in both kidneys. However, ischemia resulted in impaired distal acidification as judged by three separate maneuvers: minimal urinary pH following sulphate infusion was higher in ischemic than in control kidney (6.61 +/- 0.39 vs. 5.39 +/- 0.26, P less than 0.01), mean urine to blood PCO2 difference (U-B PCO2) was significantly lower during phosphate infusion (ischemic: 13.8 +/- 4.1 mm Hg, control: 37.2 +/- 6.8 mm Hg, P less than 0.01) and was completely abolished during isotonic NaHCO3 infusion in the ischemic kidney (-1.9 +/- 3.4 mm Hg) compared to control (40.1 +/- 14.8 mm Hg, P less than 0.05). Urinary potassium excretion was intact following ischemia and was appropriately suppressed by amiloride. Administration of 0.7 M NaHCO3 solution at a rate sufficient to produce maximally alkaline urine resulted in a similar U-B PCO2/UHCO3 relationship in both kidneys in the face of impaired distal acidification in the ischemic kidney. This suggests either that the defect may be reversed by massive bicarbonate infusion or, alternatively, that U-B PCO2 difference may be related to other factors in addition to distal H+ secretion.(ABSTRACT TRUNCATED AT 250 WORDS)