DETERMINATION OF 6-KETO-PROSTAGLANDIN F1-ALPHA IN RABBIT KIDNEY AND URINE AND ITS RELATION TO SODIUM-BALANCE

The occurrence of 6‐keto‐prostaglandin Flα (6‐keto‐PGF1α) was demonstrated in rabbit kidney medulla and cortex by mass‐spectrometry. The post‐mortem accumulation of 6‐keto‐PGF1α was studied by mass‐fragmentography in regions of the rabbit kidney using (3,3,4,4,‐2H4) 6‐keto‐PGFlα as an internal standard. The cortex contained 1.4 + 0.3 μMg/g, the medulla 2.1 ± 0.6 μg/g and the papilla 3.7 ± 0.7 (S.E.) μg/g. The accumulation of 6‐keto‐PGF1α is thus about 5 fold higher in the cortex than reported for PGE2 and PGF2α, whereas accumulation of PGE2 and PGF2α dominates over 6‐keto‐PGFlα in the medulla and the papilla. The occurrence of 6‐keto‐PGFlα in rabbit urine was demonstrated by mass‐fragmentography. On a low salt diet unanesthetized, female rabbits (n = 6) excreted Na+ 0.09 ± 0.01 (S.E.) mmol/day, 6‐keto‐PGFlα 11.8 ± 2.2 μg/day and immunoreactive PGF2α (iPGF2α) 2.0 ± 0.6 μg/day. Two days treatment with acetylsalicylic acid (30 mg/kgx 2) reduced urinary excretion of 6‐keto‐PGFlα and iPGF2α by 71 and 85%, respectively (both p < 0.05), but sodium excretion was unchanged. On the same diet supplemented with NaCl, the rabbits excreted Na+ 27.5 ± 3.4 mmol/day (p < 0,05), 6‐keto‐PGFlα 13.3 ± 4.6 μg/day (p > 0.05) and iPGF2α 0.63 ± 0.10 μg/day (p < 0.05). 6‐keto‐PGFlα is a major metabolite of prostacyclin (PGI2). The occurrence of 6‐keto‐PGFlα in kidney and urine indicates a considerable synthesis of PGI2 in the kidney. The data on urinary PG excretion indicate that intrarenal synthesis of PGI2, in contrast to PGF2α, is not influenced by dietary variations in NaCl. © 1979 Scandinavian Physiological Society