Prostaglandin F(2α) reduces intraocular pressure possibly by increasing uveoscleral outflow. To further understand the mechanism of its action binding sites for prostaglandin F(2α) and, for comparison, prostaglandin E2 were localised in sections of human cadaveric eyes using an in vitro ligand-binding technique and autoradiography. Specific binding sites for both prostaglandin F(2α) and E2 were co-localised at a high level in the areas of the ciliary muscles and iris sphincter muscles, and at a lower level in the iris epithelium and the retina. The results suggest that prostaglandin F(2α) and also prostaglandin E2, could modulate uveoscleral outflow by binding to their receptors located on the ciliary muscles and inducing their relaxation.
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience