Determination oi 6‐keto‐prostaglandin F_lα in rabbit kidney and urine and its relation to sodium balance

Abstract

Abstract The occurrence of 6‐keto‐prostaglandin F lα (6‐keto‐PGF 1α ) was demonstrated in rabbit kidney medulla and cortex by mass‐spectrometry. The post‐mortem accumulation of 6‐keto‐PGF 1α was studied by mass‐fragmentography in regions of the rabbit kidney using (3,3,4,4,‐ 2 H 4 ) 6‐keto‐PGF lα 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‐PGF 1α is thus about 5 fold higher in the cortex than reported for PGE 2 and PGF 2α , whereas accumulation of PGE 2 and PGF 2α dominates over 6‐keto‐PGF lα in the medulla and the papilla. The occurrence of 6‐keto‐PGF lα 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‐PGF lα 11.8 ± 2.2 μg/day and immunoreactive PGF 2α (iPGF 2α ) 2.0 ± 0.6 μg/day. Two days treatment with acetylsalicylic acid (30 mg/kgx 2) reduced urinary excretion of 6‐keto‐PGF lα and iPGF 2α 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‐PGF lα 13.3 ± 4.6 μg/day (p > 0.05) and iPGF 2α 0.63 ± 0.10 μg/day (p < 0.05). 6‐keto‐PGF lα is a major metabolite of prostacyclin (PGI 2 ). The occurrence of 6‐keto‐PGF lα in kidney and urine indicates a considerable synthesis of PGI 2 in the kidney. The data on urinary PG excretion indicate that intrarenal synthesis of PGI 2 , in contrast to PGF 2α , is not influenced by dietary variations in NaCl.