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The mechanism of action of prostaglandins on uveoscleral outflow

Schachtschabel, Undine PhD; Lindsey, James D. PhD; Weinreb, Robert N. MD

Current Opinion in Opthalmology: April 2000 - Volume 11 - Issue 2 - p 112-115
Glaucoma
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It is generally accepted that prostaglandins (PGs) lower intraocular pressure by increasing uveoscleral outflow. The growing use of PGs to lower intraocular pressure has led to increased interest in the uveoscleral outflow. Uveoscleral outflow passes through extracellular spaces within the ciliary muscle and then through the suprachoroidal space to the posterior pole of the eye. Recent studies indicate that this reflects a direct effect of PGs on specific ciliary muscle prostanoid receptors. Activation of these receptors stimulates several linked responses, including cAMP formation and induction of c-Fos and c-Jun expression. These signals lead to increased biosynthesis of matrix metalloproteinases, a family of neutral proteinases that can cleave extracellular matrix molecules. These matrix metalloproteinases may initiate the alteration of collagens in the ciliary muscle to increase spaces among ciliary muscle fibers, thereby reducing hydraulic resistance in the uveoscleral outflow pathway.

Glaucoma Center and Department of Ophthalmology, University of California San Diego, La Jolla, California, USA

Correspondence to Robert N. Weinreb, MD, Glaucoma Center 0946, University of California San Diego, La Jolla, CA 92093, USA

© 2000 Lippincott Williams & Wilkins, Inc.