Rho kinase (ROCK) inhibitor netarsudil (Rhopressa) lowers IOP by a mechanism that is DISTINCT from other anti-glaucoma drugs. It primarily works by:
- A Relaxing trabecular meshwork and Schlemm's canal cells, enhancing conventional (trabecular) outflow ✓
- B Reducing aqueous humour production from the ciliary body
- C Constricting episcleral veins to reduce episcleral venous pressure
- D Enhancing uveoscleral outflow via FP receptor stimulation
Explanation
Netarsudil (a ROCK inhibitor) lowers IOP through multiple mechanisms but primarily by relaxing the actin cytoskeleton of trabecular meshwork cells and Schlemm's canal cells, reducing outflow resistance through the conventional (trabecular-canalicular) pathway. Additionally, it reduces episcleral venous pressure and has some effect on aqueous production. This trabecular outflow enhancement mechanism is unique — most other agents (prostaglandins: uveoscleral; beta-blockers/carbonic anhydrase inhibitors: aqueous production suppression; alpha-2 agonists: dual) do not primarily enhance conventional outflow. Fixed-dose combination with latanoprost (Rocklatan) provides complementary mechanisms.
Reference: Khurana Comprehensive Ophthalmology, 7th ed.
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Written and medically reviewed by the StethoPrep medical team.