Effects of prostaglandins on the aqueous humor outflow pathways

Robert N. Weinreb, Carol B. Toris, B'Ann T. Gabelt, James D. Lindsey, Paul L. Kaufman

Research output: Contribution to journalArticlepeer-review

200 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)S53-S64
JournalSurvey of Ophthalmology
Issue number4 SUPPL. 1
StatePublished - Aug 2002


  • Ciliary muscle
  • Collagen
  • Extracellular matrix
  • Matrix metalloproteinase
  • Prostaglandin
  • Trabecular outflow facility
  • Uveoscleral outflow

ASJC Scopus subject areas

  • Ophthalmology


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