Although prostaglandins of the E and F series have been measured in amniotic fluid from several species1−3 their principal site of synthesis remains uncertain. In man, for example, the decidua4,5 foetal membranes6,7 and myometrium8 have all been shown to synthesise prostaglandins in vitro and each may contribute to the prostaglandin composition of amniotic fluid. The foetal lung and kidneys secrete considerable volumes of fluid into the amniotic sac9,10 and hence may also contribute to the prostaglandin content of amniotic fluid. The levels of prostaglandins in foetal tracheal fluid have been shown to be much lower than those in amniotic fluid11 and it was suggested that foetal urine is a more likely source of amniotic fluid prostaglandins. The foetal kidney is capable of synthesising prostaglandins12 and there is a growing body of evidence that prostaglandins are intimately involved in renal function13−15. We have, therefore, measured the concentrations of PGE, PGF and 13, 14-dihydro-15-keto-prostaglandin F (PGFM) in foetal urine during late pregnancy in sheep and have further determined the osmolality, Na+ and K+ concentrations of foetal urine and plasma. The concentrations of prostaglandins measured in foetal urine were similar to amniotic fluid levels but significantly greater than those previously reported in plasma and tracheal fluid suggesting that the kidney is a major source of amniotic fluid prostaglandins. The excretions of prostaglandins were related to the rate of urine flow; the excretions of PGF and PGFM were correlated with osmolar and solute-free water clearances and Na+ excretion, whereas excretion of PGE was related only to the clearance of solute-free water. Prostaglandins may thus contribute substantially to renal function and volume homeostasis in foetal life.