The capacity of fetal and maternal blood vessels to synthesize the antithrombotic vasodilator agent prostacyclin (PGI2) suggests that this substance participates in the circulatory adjustments to pregnancy. We studied the capacity of fetal and maternal blood vessels to metabolize [1(-14)C]arachidonic acid; thin-layer chromatography was used to separate PGE2, PGF2alpha, and 6-keto-PGF1alpha (the stable hydrolysis product of PGI2), and these were then quantitated by scintillation counting. Fetal vascular tissues (aorta, ductus arteriosus, and pulmonary arteries) generated tenfold more PGI2 than PGE2. Prostacyclin accounted for more than 50% of the prostaglandins synthesized by fetal blood vessel measured by recovery of its hydrolysis product, 6-keto-PGF1alpha. In contrast, in the mature animals, the aorta and pulmonary artery generated less PGI2 than did fetal tissue, whereas the mesenteric arteries exhibited high biosynthetic capacity comparable to that of the fetal vasculature. Release of prostaglandins by the umbilical blood vessels and ductus arteriosus was also measured by mass fragmentography. The identity of 6-keto-PGF1alpha was confirmed by mass spectroscopy. The high and almost identical capacity of all fetal blood vessels, except the umbilical arteries and veins, to synthesize PIG2 could reflect an important role for this prostaglandin in the regulation of the fetal circulation.