Nilvadipine Inhibits Acute Rise of Aqueous Flare and Intraocular Pressure Induced by Prostaglandin E ₂ in Pigmented Rabbits

Abstract

To evaluate the possible role of calcium channel blocker on changes in aqueous flare and intraocular pressure induced by prostaglandin E₂ (PGE₂) in pigmented rabbits, we examined the effects of nilvadipine and nicardipine (calcium channel blockers). PGE₂, 25 µg/ml, was administered using a glass cylinder. Nilvadipine or nicardipine was injected intravenously. Aqueous flare was measured by a laser flare cell meter. Intraocular pressure was measured by a noncontact tonometer. After administration of PGE₂, aqueous flare and intraocular pressure increased and then decreased. Increased flare and elevated intraocular pressure following PGE₂ administration were inhibited by nilvadipine in a dose-dependent manner (5–500 µg/kg body weight). These responses were inhibited only slightly by nicardipine at the same concentration. Nilvadipine injected 30 min before PGE₂ application inhibited the increase maximally. The inhibitory effect was found on days 1, 3, 5, and 7 by daily administration of nilvadipine. A good correlation between the inhibition of intraocular pressure and the inhibition of increased flare by nilvadipine was found. We believe that Ca²⁺, or calcium channel blocker-related substances may be involved in the mechanism of PGE₂-induced elevation of aqueous flare and intraocular pressure in the pigmented rabbit.