Current pharmacological therapies for lowering the intraocular pressure in glaucoma include increasing aqueous humor outflow and suppression of aqueous humor production. For example, aqueous humor production is reduced by both topical and systemic carbonic anhydrase inhibitors which decrease the production of aqueous humor by the epithelial cells of the ciliary body. Aqueous humor outflow is increased by prostaglandin agonists that increase outflow mainly through the uveoscleral pathway, possibly through the activation of matrix metalloproteinases, and also through the trabecular meshwork. Other glaucoma medications such as adrenergic agonists decrease outflow resistance through mechanisms that are not completely clear.

Current surgical therapies also seek to lower the intraocular pressure by increasing aqueous outflow or decreasing aqueous humor production. For example, ciliary body ablative laser treatments such as cyclcophotocoagulation laser (either transcleral or endopscopic) seek to partially destroy the cililary body to decrease aqueous production. In contrast, laser trabeculoplasty modifies the trabecular meshwork (in a manner still not known) to decrease outflow resistance. Other surgeries such as trabeculectomy, glaucoma drainage implants, and glaucoma shunts (which penetrate the trabecular meshwork and cannulate Schlemm’s canal or create a path through the scleral wall) bypass outflow resistance by shunting aqueous humor through or around the trabecular meshwork. Newer procedures such as canaloplasty (which dilates Schlemm’s canal) and other shunts which seek to open the uveoscleral pathway by creating a mini-cyclodialysis cleft all involve increasing outflow by opening existing aqueous drainage pathways or creating new pathways.