Mechanism of Action
Ocular hypotensive prostaglandin analogues are prodrugs that penetrate the cornea and become biologically active after being hydrolyzed by corneal esterase. These drugs lower IOP by increasing aqueous humor outflow via the uveoscleral pathway and decreasing outflow resistance. The precise mechanism by which these changes occur has not been fully determined. It is thought that the ocular hypotensive prostaglandin analogues bind to various prostaglandin receptors, most importantly prostaglandin F2α (PGF2α), triggering a cascade of events that lead to activation of matrix metalloproteinases. This in turn leads to remodeling of the ciliary body, trabecular meshwork, and possibly scleral extracellular matrix, so that the flow rate of aqueous humor through these tissues is increased. Topical prostaglandin analogue therapy results in increased space between the muscle fascicles within the ciliary body, which is thought to be the primary location of uveoscleral outflow.
Table 12-2 Glaucoma Medications
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.