Comparison of PGE2, 6‐keto PGF1αand renin release from dog kidneys

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Abstract
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. PGI2was measured as its stable hydrolysed product, 6‐keto PGF1α. The two former procedures raised PGE2release to 13 ± 2 pmol min‐1, 6‐keto PGF1αrelease to 5 ± 2 pmol min‐1and renin release to 23 ± 5 μg AI min‐1, Angiotensin II infusion, reducing the renal blood flow by 30%, increased PGE2and 6‐keto PGF1αrelease 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 PGE2and 6‐keto PGF1αrelease did not increase further in any of the experiments. Arachidonic acid, infused at 40 and 160 μg kg‐1min‐1, increased prostaglandin release in proportion to the infusion rate. At the highest infusion rate, PGE2release averaged 166± 37 pmol min‐1and 6‐keto PGF1αrelease 98 ± 28 pmol min‐1. All procedures increased PGE2and 6‐keto PGF1αrelease in a fixed proportion of about 2.5:1, whereas renin release increased only during autoregulatory vasodilation.