Early proximal convoluted tubules were perfused in vivo with equilibrium Ringer buffered at pH 7.65 and 6.5 to characterize phosphate absorption due to changes in extracellular and intracellular hydrogen ion concentration. Phosphate absorption is normally greater from intraluminal pH 7.65 compared with pH 6.5 in thyroparathyroidectomized rats with fractional phosphate excretion of 0.5%. Metabolic alkalosis produced by bicarbonate infusion in rats ingesting normal amounts of phosphate (45 mg/day) resulted in an increase in overall renal phosphate reabsorption (fractional phosphate excretion 0.3%). The Jmax and Km values were: pH 7.65, 33.67 +/- 13.49 pmol X min-1 X mm-1, and 1.74 +/- 0.30 mM; pH 6.5, 24.87 +/- 6.22 and 0.50 +/- 0.25, respectively. By contrast, rats on a high dietary phosphate intake (180 mg/day) demonstrated a large increase in urinary phosphate excretion (18%) following bicarbonate infusion, which was due to a decrease in tubular phosphate absorption from both alkaline and acidic luminal pH values. Acute metabolic acidosis did not significantly alter tubular transport at either intraluminal pH value. In contrast, rats maintained on an elevated dietary acid intake for 5 days had a phosphaturia (fractional excretion 7.1%) and diminished reabsorptive capacity. Dietary acidosis also decreased tubular phosphate transport in rats previously maintained on phosphate-restricted diets. These data suggest that acid-base balance may modulate tubular phosphate transport independent of intraluminal pH and phosphate concentration. Further, these changes depend on the chronicity of exposure and act independent but integral to the effects of parathyroid hormone and the intrinsic adaptation to dietary phosphate availability.