We examined the disruption of the blood-aqueous barrier following prostaglandin (PG)-E2 application in rabbits. Vehicle or PGE2 in 10, 50 or 250 μg/ml concentration was applied to the cornea of pigmented rabbit with the use of a glass cylinder. After PGE2 administration, horseradish peroxidase (HRP) was injected intravenously. Then the eyes were enucleated, and distribution of HRP in the anterior segments was examined by electron microscopy. In control eyes, diffusion of HRP was blocked by vascular endothelial cells in the iris and by nonpigmented epithelial cells in the iridial and ciliary processes. In the iridial and ciliary processes of the eyes treated with 10 μg/ml PGE2, no HRP reaction product was seen in intercellular spaces of the nonpigmented epithelial cells, but it was found in pinocytotic vesicles. In the eyes treated with 50 μg/ml PGE2 HRP reaction product was found in intercellular spaces of the nonpigmented cells in the iridial processes. In the eyes treated with 250 μg/ml PGE2 HRP reaction product was further distributed in the iris stroma. The present study demonstrated that the sites of breakdown of the blood-aqueous barrier depended upon the doses of exogenous PGE<sub>2</sub>.