The effects of urine flow rate and urinary pH on renal prostaglandin E2 (PGE2) and kallikrein excretion were investigated in conscious dogs during water deprivation followed by rehydration and under conditions which altered urine pH, but caused similar change in salt and water excretion. 2. When water-restricted dogs were rehydrated in two steps by gavage giving the animals tap water, urine flow increased by 22- and 63-fold with a concomitant increase in PGE2 excretion by 100 and 318%, respectively; whereas urinary kallikrein excretion and urine pH did not change significantly. 3. Oral administration of isotonic sodium chloride solution increased urine flow as well as electrolyte excretion without altering urine pH (6.90 +/- 0.26) and PGE2 excretion. 4. When urine was made alkaline (pH 7.79 +/- 0.09) by oral sodium bicarbonate, urine flow and electrolyte excretion were similar to those observed after oral sodium chloride, while renal PGE2 excretion increased by 66% (P less than 0.05). 5. When urine was made acidic (pH 5.31 +/- 0.14) by oral ammonium chloride, urine flow and electrolyte excretion were similar to the values seen after oral sodium chloride. Urinary PGE2 excretion, however, was reduced by 46% (P less than 0.05). 6. After oral fluid loads a positive correlation could be detected between urine pH and urinary PGE2 excretion (r = 0.854, P less than 0.001). 7. Urinary kallikrein excretion was not significantly altered by any of the three interventions mentioned above. 8. The present results suggest that, in conscious dogs, urine flow as well as urine pH are important determinants of urinary PGE2 excretion rates, but not of kallikrein excretion.
