Renal degradation and distribution between urinary and venous output of prostaglandins E2 and I2.

To examine renal degradation and distribution between urine and renal venous blood, prostaglandins E2 and I2 (PGE2 and PGI2), and a metabolite of PGI2, 6-keto-PGF1 alpha, were infused into the suprarenal aorta of anaesthetized dogs after blocking prostaglandin synthesis by indomethacin, 10 mg kg-1 body wt iv. During one passage through the kidney 80% of PGE2 and only 25% of PGI2 and 6-keto-PGF1 alpha were metabolized. Prostaglandin degradation and arterial input were proportional (r greater than 0.90). To stimulate the intrarenal prostaglandin synthesis in unblocked kidneys, arachidonic acid was infused at rates ranging from 24 to 160 micrograms min-1 kg-1 body wt. During arachidonic acid and PGE2 infusion the urinary excretion of PGE2 was about 20% of the renal venous output over a wide range of infusion rates. During arachidonic acid and PGI2 infusion urinary excretion of 6-keto-PGF1 alpha was about 10% of total renal output, but failed to increase further when total renal output exceeded 70 pmol min-1. Further increase in output occurred only in the renal vein. In contrast, during 6-keto-PGF1 alpha infusion the urinary excretion and the renal venous output of this metabolite were related as 1:2 over a wide range of infusion rates. Thus, PGI2 is much less degraded by renal tissue than PGE2, and the distribution patterns differ. Similar distributions between urine and renal venous blood during aortic infusion and stimulated intrarenal synthesis suggest a pre-glomerular vascular origin of both prostaglandins.