During parturition, Ferguson's reflex is a positive feedback mechanism: fetal head pressure on the cervix stimulates oxytocin release from the posterior pituitary, which increases uterine contractions, further pushing the head against the cervix. Why does uterine sensitivity to oxytocin increase dramatically at term compared to early pregnancy?

• A Placental steroid production shifts from progesterone dominance to estrogen dominance at term, and estrogen upregulates myometrial oxytocin receptors ✓
• B Fetal cortisol decreases placental CRH production, removing the inhibitory effect on uterine oxytocin receptors
• C Increased fetal ADH production at term cross-reacts with uterine oxytocin receptors because they are structurally similar
• D Cervical ripening by relaxin increases gap junctions in the myometrium which amplify oxytocin receptor signaling

Explanation

Throughout pregnancy, progesterone dominance suppresses myometrial excitability and keeps oxytocin receptor (OTR) expression low. As term approaches, the estrogen-to-progesterone ratio rises (partly due to placental estrogen production and relative progesterone withdrawal at the receptor level in humans, mediated by progesterone receptor isoform B→A shift). Estrogen strongly upregulates OTR expression in the myometrium — a 100–200× increase near term — and also increases gap junction (connexin 43) expression for electrical coupling of myometrial cells. This orchestrated upregulation makes the uterus exquisitely sensitive to oxytocin and enables the progressive positive feedback of the Ferguson reflex during active labor.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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Written and medically reviewed by the StethoPrep medical team.