The "E" series of prostaglandins are responsible for maintaining the openness of the ductus arteriosus (by dilation of vascular smooth muscle) throughout the fetal period.

[6] Immediately after birth, the levels of both PGE2 and the EP4 receptors reduce significantly, allowing for closure of the DA and establishment of normal postnatal circulation.

[6] Ductus arteriosus closure may be induced by administration of nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit prostaglandin production.

[8] In some types of congenital heart defect (e.g., transposition of the great arteries), prostaglandins may be administered to maintain the DA open, allowing for the continual circulation and oxygenation of blood, until surgery can be performed.

During embryonic development, reptiles, birds, and mammals all have either one or two paired ductus arteriosi that provide a fetal shunt of blood away from the lungs.