The preovulatory LH surge triggers ovulation through a cascade involving prostaglandin production in the follicle. Which specific event is immediately responsible for follicular rupture?

• A LH directly activates FSH receptors on the oocyte, inducing resumption of meiosis I and mechanical pressure that ruptures the follicle
• B Estradiol surge immediately before LH peak activates oxytocin receptors on the follicle, causing smooth muscle contraction that squeezes out the cumulus-oocyte complex
• C The LH surge increases intrafollicular pressure by stimulating fluid secretion until the follicular wall bursts at the stigma
• D PGE2 and PGF2α stimulate matrix metalloproteinases (MMPs) and plasminogen activators that degrade the follicular wall, with simultaneous smooth muscle contraction expelling the oocyte ✓

Explanation

The LH surge triggers multiple proteolytic events at the follicular apex (stigma). LH stimulates granulosa cells to produce prostaglandins (PGE2 via COX-2 induction) and activates tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA), which generate plasmin. Plasmin and MMPs (MMP-1, MMP-9) degrade collagen and proteoglycans in the follicular basement membrane and theca layer. This enzymatic dissolution weakens the follicular wall at the stigma, while surrounding smooth muscle cells (stimulated by prostaglandins) contract to expel the cumulus-oocyte complex. COX-2 inhibitors (NSAIDs) can impair ovulation by blocking prostaglandin synthesis — a relevant clinical consideration.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.