A newborn's PaO2 rises from 25 mmHg (fetal) to 95 mmHg after birth. This rise in PaO2 causes closure of the ductus arteriosus primarily by which mechanism?
- A Increased O2 inhibits vascular smooth muscle KATP channels, causing depolarization and vasoconstriction
- B Bradykinin release from expanding lungs directly constricts ductal smooth muscle via B2 receptors
- C O2-sensitive Kv (voltage-gated K+) channel inhibition in ductal smooth muscle cells → membrane depolarization → Ca2+ influx via L-type channels → contraction ✓
- D Indomethacin-like effect of rising O2 tension inhibiting prostaglandin synthesis which was keeping the ductus open
Explanation
Ductal smooth muscle cells have O2-sensitive voltage-gated K+ (Kv) channels. At low fetal PO2, these channels are open, maintaining membrane hyperpolarization and ductal dilation (further potentiated by prostaglandins PGE2 and PGI2). When PaO2 rises after birth, O2 directly inhibits these Kv channels → K+ efflux decreases → membrane depolarizes → L-type Ca2+ channels open → [Ca2+]i rises → contraction and ductal closure. Prostaglandin withdrawal (from loss of placental PGE2 and rise in O2 inhibiting local COX) augments but is not the primary acute mechanism. KATP channels are the mechanism in pancreatic beta cells and some vascular beds, but not the dominant ductal mechanism.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.