1. The influence of oral water loading on the excretion rate of prostaglandin (PG) E was investigated in healthy human subjects in a control study where the urine was acidic (pH 5.7) and after oral sodium bicarbonate, which made the urine mildly alkaline (pH 7.2). PGE was immediately extracted from urine and measured by a radioimmunoassay technique. 2. After sodium bicarbonate (5 g) the urinary PGE excretion rate was some three-fold higher ( P < 0.01) than in the control study, in the absence of any significant difference in the urine flow (approximately 80 ml/h). 3. In the control study (urine pH 5.7) the urinary PGE excretion rate increased significantly ( P < 0.01) as the urine flow rose in response to the oral fluid load. However, after sodium bicarbonate, PGE excretion did not alter after the fluid load despite a 10-fold increase in urine flow. 4. Since after bicarbonate administration PGE excretion is independent of urine flow, mildly alkaline urine may represent a condition under which renal PGE synthesis can be effectively assessed from measurements of urinary PGE excretion, in the presence of changes in urine flow. 5. In addition, the results are compatible with the hypothesis that, in man, PGE may be passively reabsorbed in the distal nephron, and a reduction in this reabsorption could contribute to or be responsible for the dependency of the excretion rate of PGE on urine flow.
1. The urinary excretion of prostaglandin E 2 (PGE 2 ) was measured in conscious rats under conditions which produced either acid or alkaline urine, but similar change in fluid and solute excretion. 2. Oral isotonic saline increased both urine flow and sodium excretion but did not alter urinary PGE 2 output (which remained constant at 80 pmol/3 h per rat) or urine pH (6.2). 3. When the urine was made alkaline (pH 7.8) by oral sodium bicarbonate or carbonate, urinary PGE 2 was approximately 3-fold greater (P<0.00l) than the control (pH6.2). The urine flow and sodium output were also increased. 4. When the urine was made acidic (pH 5.7) by oral ammonium chloride, urinary PGE, excretion was reduced (P<0.01) to approximately half the control output. The urine flow and sodium output increased. 5. Within a group of 12 rats receiving oral isotonic saline a positive linear correlation coefficient (P<0.002) was established between urine pH and PGE2 excretion. 6. The results indicate that urine pH may be a determinant of PGE2 excretion in unrestrained, conscious rats. It seems likely that this effect of pH is mediated by a change in the passive reabsorption of PGE, in the distal nephron, although alternative explanations such as altered tubular secretion or synthesis cannot be categorically excluded.