Mechanism of volume expansion on citrate, ammonia, and acid excretion in the rat.

Potassium-depleted rats receiving sodium chloride or i.v. mannitol decrease their blood bicarbonate concentration isohydrically, reduce urinary citrate, and increase urinary ammonia excretion per milligram of urinary creatinine. To determine the mechanisms of these renal changes, we volume expanded normal rats with mannitol, normal saline, or saline bicarbonate solutions. Blood pH in each group remained constant, but blood bicarbonate fell significantly in the mannitol and saline-infused rats. In these two groups, urinary citrate per unit GFR decreased 27% and 25% (P less than 0.01) but urinary ammonia excretion per unit GFR increased 120% and 90% (P less than 0.01). By contrast, in saline bicarbonate rats, citrate excretion increased 27% and urinary ammonia excretion rose 29% (P greater than 0.2). Rats with metabolic acidosis given saline did not alter blood pH or bicarbonate. Citrate excretion per unit GFR increased 150% (P less than 0.02) but urinary ammonia excretion rose insignificantly by 11%. Calculated net tubular reabsorption of citrate increased in the mannitol and saline-infused rats. The rise in urinary pH in these two groups during expansion suggest that renal ammonia production was also increased. We conclude that volume expansion changes renal citrate and ammonia metabolism by isohydrically reducing blood bicarbonate concentration, thereby demonstrating another effect of bicarbonate, independent of pH, on renal metabolism.