• 1 January 1981
    • journal article
    • research article
    • Vol. 20  (6) , 726-732
Abstract
A disruption of the blood-aqueous barrier in rabbit eyes was elicited by use of topical prostaglandin E2(PGE2), IR irradiation of the iris or by s.c. .alpha.-melanocyte-stimulating hormone (.alpha.-MSH). The aqueous flare provoked was measured quantitatively with a photoelectric instrument. The effect of the (topical) .beta.-adrenergic antagonist timolol maleate on the breakdown of the blood-aqueous barrier was tested. Timolol applied topically in very large doses had no effect on exogenously administered PGE2. Even in a very small concentration applied topically, timolol reduced the flare response to both IR irradiation and .alpha.-MSH. The effect of .alpha.-MSH and IR irradiation on the blood-aqueous barrier is dependent on intact .beta.-adrenergic receptor sites.