It seems likely that prostaglandins play a significant part in the mechanisms of parturition both at term and preterm. Concentrations of prostaglandins are increased in the blood, urine and amniotic fluid during labour. There are differences in the concentrations of prostaglandins in amniotic fluid from the forebag and hindbag. Nevertheless, if liquor is sampled only from the hindbag a highly significant increase in prostaglandin concentrations occurs throughout labour. Furthermore, we now have evidence that prostaglandin concentrations in amniotic fluid increase before the onset of labour. Prostaglandins are synthesized by uterine tissues and increased rates of production occur during labour. The amnion, chorion and decidua all contain mRNA for the newly-discovered inducible form of prostaglandin H synthase (PGHS-2) as well as mRNA for the constitutive form (PGHS-1). Using the reverse transcription polymerase chain reaction (RT-PCR) both mRNAs can be detected during late pregnancy whether women are in labour or not. PGHS-2 protein is detected by Western blot analysis in cells derived from all three tissues. There is regulation of PGHS-2 protein amounts by cytokines, phorbol esters and growth factors. For example, in amnion cells interleukin-1 beta induces a rapid increase in PGHS-2 mRNA levels followed by a decrease to undetectable levels within 4 h of treatment; PGHS-2 protein amounts are also elevated by this treatment. Administration of prostaglandins will induce labour and delivery, whereas inhibition of prostaglandin biosynthesis will delay labour and delivery. Hence, increased prostaglandin production is likely to be a key determinant of the onset and progression of the parturient process.