The mechanism by which brimonidine (alpha-2 agonist) lowers IOP differs from that of timolol primarily in that brimonidine:

• A Reduces aqueous production AND increases uveoscleral outflow, while timolol only reduces aqueous production via beta-2 receptor blockade ✓
• B Reduces aqueous production by inhibiting Na+/K+-ATPase in the ciliary body epithelium exclusively
• C Constricts the pupil, mechanically widening the trabecular meshwork spaces
• D Reduces episcleral venous pressure by vasoconstriction of episcleral vessels

Explanation

Brimonidine (alpha-2 adrenergic agonist) has a dual mechanism: (1) reduces aqueous production by activating presynaptic alpha-2 receptors on the ciliary epithelium, reducing cAMP and Na+/K+-ATPase activity (adenylyl cyclase inhibition); and (2) increases uveoscleral outflow — the alpha-2 receptor in the ciliary muscle relaxes the muscle, increasing the spaces between ciliary muscle bundles and enhancing uveal-scleral drainage. Timolol (non-selective beta-blocker) reduces aqueous production by blocking beta-2 receptors on the non-pigmented ciliary epithelium (reducing cAMP), but does not significantly affect uveoscleral outflow. This dual mechanism of brimonidine provides additive IOP reduction when combined with timolol, explaining the rationale for fixed-dose combinations.

Reference: Khurana Comprehensive Ophthalmology, 7th ed.

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Written and medically reviewed by the StethoPrep medical team.