Renal venous and urinary PGE2 output during intrarenal arachidonic acid infusion in dogs

Inferences about total renal (venous and urinary) PGE₂ output from determinations of urinary excretion rates (U_PGE2V) cannot be made unless the distribution of PGE₂ between renal venous plasma and urine is known. Therefore, in the present study on intact kidneys of anesthetized dogs both urinary excretion of PGE₂ and the renal venous output (the product of plasma flow and venous concentration of PGE₂) was determined during low and high rates of renal PGE₂ synthesis. PGE₂ was measured in urine and arterial and renal venous plasma by radioimmunoassay during the following conditions: (1) Hydropenia. In the control condition U_PGE2V averaged 0.041±0.012 pmol/g·min and varied between 4 and 70% of the total PGE₂ output. With infusion of arachidonic acid (AA, 160 μg/kg·min) into the renal artery total PGE₂ output increased from 0.18±0.03 to 3.23±0.51 pmol/g·min, whereas arterial concentrations of PGE₂ were unchanged. The urinary fraction still varied between 6 and 46% of total renal PGE₂ output. (2) High urine flows caused by mannitol, saline or saline and ethacrynic acid (ECA) infusion. These procedures did not stimulate total renal PGE₂ output and the urinary fraction varied between 4 and 49%. ECA combined with saline infusion increased the urinary fraction significantly to 34.7±4.0%. AA increased the total PGE₂ output as during hydropenia, but the urinary fraction fell to 13% in 13 dogs and was unchanged at about 8% in six dogs. On average the urinary fraction of total PGE₂ output was significantly lower than in hydropenia. Thus, the urinary fraction of total renal PGE₂ output is not constant, and urinary excretion of PGE₂ does not give reliable information about renal synthetic rates of prostaglandins.