At birth, the ductus arteriosus begins to close within hours. Which of the following is the MOST important trigger for functional closure of the ductus arteriosus?
- A Rise in arterial PO2 after the onset of pulmonary ventilation, causing smooth muscle contraction in the ductal wall ✓
- B Increase in prostaglandin E2 production stimulated by the first breath
- C Removal of maternal progesterone withdrawing its relaxant effect on ductal smooth muscle
- D Bradykinin released from pulmonary vasculature acting on ductal smooth muscle receptors
Explanation
The ductus arteriosus remains patent in fetal life primarily because low PO2 (fetal arterial PO2 ~25–35 mmHg) inhibits oxygen-sensitive K⁺ channels in ductal smooth muscle, promoting membrane depolarization, Ca²⁺ entry, and vasodilation. Additionally, PGE2 and PGI2 from the placenta maintain patency. At birth, lung expansion raises arterial PO2 to ~100 mmHg, which opens K⁺ channels, hyperpolarizes ductal smooth muscle, reduces Ca²⁺ influx, and causes contraction — functional closure within hours. PGE2 (option B) maintains patency prenatally and falls after birth; indomethacin (a prostaglandin inhibitor) is used to close a patent ductus, confirming option B's direction is backward. Progesterone withdrawal (option C) is relevant to uterine contraction, not ductal closure.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.