We studied the effects of furosemide on urinary excretion of PGE2 and sodium and the effects of inhibition of prostaglandin (PG) synthesis with indomethacin or furosemide-induced PGE2 excretion and natriuresis in normal man. Furosemide (20 mg i.v.) increased the urinary excretion of PGE2 from 71.2 ± 17.2 to 255.9 ± 41.0 ng/4 h. Sodium excretion increased in parallel. Indomethacin, in a dose sufficient to decrease basal urinary PGE2 excretion by 〉90%, significantly decreased both urinary PGE2 and sodium excretion under furosemide without affecting delivery of furosemide into the urine. The urinary excretion of furosemide was 9.4 ± 0.4 and 9.3 ± 1.4 mg/24 h with and without indomethacin, respectively. However, the furosemide-induced encrement in PGE2 excretion and sodium excretion over baseline was not changed. Furosemide-stimulated urinaary PGE2 excretion correlated significantly with sodium excretion rate with and without indomethacin. Indomethacin changed the relationship between absolute amounts of furosemide in urine and PGE2 excretion but did not affect the increment in excretion over baseline or the significant correlation of urinary PGE2 with sodium excretion.
- Prostaglandin E
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