At birth, the ductus arteriosus closes functionally. Which mediator is responsible for its postnatal closure, and which agent keeps it patent antenatally?
- A Oxygen (rise in PaO2 causes closure); prostaglandin E2 (PGE2) keeps it patent antenatally ✓
- B Bradykinin causes closure; nitric oxide keeps it patent
- C Endothelin-1 causes closure; prostacyclin keeps it patent
- D Angiotensin II causes closure; PGI2 keeps it patent
Explanation
The ductus arteriosus remains patent in fetal life primarily due to prostaglandin E2 (PGE2) and low oxygen tension — hence indomethacin (a COX inhibitor reducing PGE2) is used to close a patent ductus arteriosus (PDA) medically in preterm neonates. At birth, the rise in arterial oxygen tension triggers smooth muscle contraction and functional closure within hours; anatomical closure (fibrosis → ligamentum arteriosum) occurs within weeks. This is why prostaglandin E1 (alprostadil) infusion is used to keep the ductus open in ductus-dependent congenital heart defects.
Reference: BD Chaurasia's Human Anatomy, 8th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.