Prostaglandin F2α and its analogues are the most potent and efficacious topical ocular hypotensive agents currently known.1-7 Their hypotensive action results primarily, if not exclusively, from enhancement of uveoscleral drainage of aqueous humor,8,9 in turn consequent to relaxation of the ciliary muscle10-12 and remodeling of the connective tissue between the outer longitudinal muscle bundles.13-15 The latter probably results from prostaglandin-stimulated induction of matrix metalloproteinase enzymes.16
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Prostaglandins are autacoids, ie, hormones that are synthesized and released, act locally,17 and probably play a role in the normal endogenous regulation of aqueous outflow. They are produced by human trabecular endothelial18 and ciliary muscle cells19 in culture and are released by various ocular tissues during many types of ocular inflammation.17 During such inflammatory episodes, the trabecular meshwork could be impaired directly by the inflammatory process or obstructed by cellular debris
Kaufman PL. Prostaglandins and Cholinomimetics. Arch Ophthalmol. 1997;115(7):911–913. doi:10.1001/archopht.1997.01100160081013
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