Comparison of PGE2, 6-keto PGF1 alpha and renin release from dog kidneys

Several renal cell types synthesize prostaglandin E2 (PGE2) and prostacyclin (PGI2). To examine whether the release of these prostaglandins varies in proportion, prostaglandin synthesis was stimulated in anaesthetized dogs by renal arterial constriction, ureteral occlusion, intrarenal angiotensin II infusion and infusion of arachidonic acid, the precursor of PG synthesis. PGI2 was measured as its stable hydrolysed product, 6-keto PGF1 alpha. The two former procedures raised PGE2 release to 13 +/- 2 pmol min-1, 6-keto PGF1 alpha release to 5 +/- 2 pmol min-1 and renin release to 23 +/- 5 micrograms AI min-1. Angiotensin II infusion, reducing the renal blood flow by 30%, increased PGE2 and 6-keto PGF1 alpha release only half as much as ureteral and renal arterial constriction, and exerted no significant effect on renin release. By increasing the infusion rate of angiotensin II up to 10 times, the renal blood flow remained unaltered in four dogs and fell to 50% of control in two dogs, but PGE2 and 6-keto PGF1 alpha release did not increase further in any of the experiments. Arachidonic acid, infused at 40 and 160 micrograms kg-1 min-1, increased prostaglandin release in proportion to the infusion rate. At the highest infusion rate, PGE2 release averaged 166 +/- 37 pmol min-1 and 6-keto PGF1 alpha release 98 +/- 28 pmol min-1. All procedures increased PGE2 and 6-keto PGF1 alpha release in a fixed proportion of about 2.5:1, whereas renin release increased only during autoregulatory vasodilation.