Rho-kinase (ROCK) inhibitors such as netarsudil lower IOP primarily through which mechanism distinct from all other current glaucoma drug classes?
- A Decreased aqueous production by inhibiting carbonic anhydrase in ciliary epithelium
- B Increased uveoscleral outflow by relaxing ciliary muscle
- C Increased trabecular meshwork outflow by cytoskeletal relaxation of trabecular cells ✓
- D Increased trabecular meshwork and Schlemm's canal permeability via norepinephrine transporter inhibition
Correct answer: C. Increased trabecular meshwork outflow by cytoskeletal relaxation of trabecular cells
Explanation
ROCK inhibitors (netarsudil) work by relaxing the actin-myosin cytoskeleton of trabecular meshwork cells, reducing their stiffness and increasing conventional (trabecular) outflow — a mechanism unique among glaucoma drugs. Netarsudil also inhibits the norepinephrine transporter, reducing episcleral venous pressure. Prostaglandins increase uveoscleral outflow; beta-blockers and CAIs reduce aqueous production; pilocarpine contracts ciliary muscle increasing trabecular outflow through a different mechanism.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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