The mechanism by which rho-kinase (ROCK) inhibitors such as netarsudil lower intraocular pressure differs from prostaglandin analogues in that they act primarily on which pathway?

• A Increased aqueous outflow via uveoscleral pathway by relaxing ciliary muscle
• B Increased trabecular meshwork outflow by reducing actomyosin contractility and reducing episcleral venous pressure ✓
• C Decreased aqueous production by inhibiting carbonic anhydrase
• D Increased outflow by dilating Schlemm's canal through prostaglandin receptors

Explanation

ROCK inhibitors (e.g., netarsudil) lower IOP via two complementary mechanisms: they relax the trabecular meshwork by inhibiting actomyosin contraction (improving conventional outflow), and they reduce episcleral venous pressure. This contrasts with prostaglandin analogues (e.g., latanoprost), which increase uveoscleral (unconventional) outflow by upregulating metalloproteinases in the ciliary muscle stroma. ROCK inhibitors are the only class that addresses the dysfunctional trabecular meshwork directly and can be combined with latanoprost (Rocklatan = netarsudil + latanoprost fixed combination).

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

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Written and medically reviewed by the StethoPrep medical team.