Survey of Ophthalmology
Volume 47, Supplement 1 , Pages S53-S64, August 2002

Effects of Prostaglandins on the Aqueous Humor Outflow Pathways☆

  • Robert N Weinreb, MD

      Affiliations

    • Corresponding Author InformationReprint address: Robert N. Weinreb, MD, Glaucoma Center, University of California San Diego, 9500 Gilman Drive 0946, La Jolla, CA 92093-0946, USA
    • Glaucoma Center, University of California San Diego, La Jolla, CA USA
    • ,
  • Carol B Toris, PhD

      Affiliations

    • Department of Ophthalmology, University of Nebraska Medical Center, Omaha, NE USA
    • ,
  • B'Ann T Gabelt, MS

      Affiliations

    • Department of Ophthalmology, University of Wisconsin, Madison, WI, USA
    • ,
  • James D Lindsey, PhD

      Affiliations

    • Glaucoma Center, University of California San Diego, La Jolla, CA USA
    • ,
  • Paul L Kaufman, MD

      Affiliations

    • Department of Ophthalmology, University of Wisconsin, Madison, WI, USA

Abstract 

Topical treatments with certain prostaglandins (PGs), including FP receptor agonists, lower intraocular pressure by increasing uveoscleral outflow. Although the precise mechanism for the increased uveoscleral outflow is not known, there appears to be activation of a molecular transduction cascade and an increase in the biosynthesis of certain metalloproteinases. This leads to reduction of extracellular matrix components within the ciliary muscle, iris root, and sclera. It is possible that this reduction of extracellular matrix present within portions of the uveoscleral pathway may contribute to the mechanism of increased uveoscleral outflow. Additional mechanisms that may contribute to the PG-mediated increase of uveoscleral outflow include relaxation of the ciliary muscle, cell shape changes, cytoskeletal alteration, or compaction of the extracellular matrix within the tissues of the uveoscleral outflow pathway. Future studies should clarify the importance of these various responses that may contribute to increased uveoscleral outflow. At present, there is no compelling evidence for a substantial facility-increasing effect on the trabecular meshwork outflow for any of these compounds.

Keywords:  ciliary muscle, collagen, extracellular matrix, matrix metalloproteinase, prostaglandin, trabecular outflow facility, uveoscleral outflow

To access this article, please choose from the options below

Login to an existing account or Register a new account.

  • Purchase this article for 31.50 USD (You must login/register to purchase this article)

    Online access for 24 hours. The PDF version can be downloaded as your permanent record.

  • Subscribe to this title

    Get unlimited online access to this article and all other articles in this title 24/7 for one year.

  • Claim access now

    For current subscribers with Society Membership or Account Number.

  • Visit SciVerse ScienceDirect to see if you have access via your institution.
 

☆ Supported in part by NIH grants EY05590 (RNW) and EY02698 (PLK) and unrestricted grants from Research to Prevent Blindness, Inc., New York, NY (University of California San Diego, University of Nebraska, University of Wisconsin). Johan Stjernschantz, M.D, Ph.D. critically reviewed the manuscript. The authors reported no proprietary or commercial interest in any product mentioned or concept discussed in this article.

PII: S0039-6257(02)00306-5

Survey of Ophthalmology
Volume 47, Supplement 1 , Pages S53-S64, August 2002

Article Tools

* Image Usage & Resolution