Abstract

Parturition is composed of five separate but integrated physiological events: fetal membrane rupture, cervical dilatation, myometrial contractility, placental separation and uterine involution. Prostaglandins (PGs) have central roles in each of these, but the most studied is myometrial contraction. Elevated uterine PGs or the enhanced sensitivity of the myometrium to PGs leads to contractions and labour. The regulator of PG synthesis is the mRNA expression of PGHS-2. Cytokines are important stimulators of this gene expression, and cortisol and other factors may be as well. This enzyme is an important therapeutic target in the prevention of preterm labour. Some preterm births occur without an elevation of uterine PGs, even though they are delayed by non-steroidal anti-inflammatory drugs (NSAIDs), suggesting enhanced myometrial sensitivity to PGs. The PGF(2alpha) receptor, FP, is emerging as a central component of uterine sensitivity and may prove to be involved with preterm birth and a reasonable target for tocolysis.