Purpose. This study investigates the role of endogenous NO in the transient IOP elevation and BAB breakdown after PG treatment in rabbits. Methods. An inhibitor of NO synthase, LNAME, was topically applied at concentrations of 1, 5 and 10% to one random eye and vehicle to the contralateral control eye of rabbits at -1, -0.5, +1.5 and +3.5 hours relative to PG administration. PGF2α (10 or 40 μg/25 μl) or PGE2 (5 μg/25 μl) was topically applied to both eyes at time zero. IOPs were measured at -0.5, 0, +0.5, +1, +2, +3 and +4 hours. In separate rabbits pretreated with 10% LNAME or vehicle, aqueous humor was collected 30 minutes after 40 μg PGF2α and assayed for protein concentration. Results. LNAME inhibited the PG-induced IOP rise in a dose-dependent manner. 10% LNAME significantly (P<0.01) blocked (100%) the IOP rise (mean±SEM) of 3.6±0.9 and 4.7±0.9 mmHg after 10 (n=5) and 40 μg (n=6) of PGF2α, respectively, and inhibited by 57% the 9.3±2.1 mmHg rise after PGE2 (n=6). LNAME inhibited the PGF2α-induced rise in aqueous protein concentration by 75% (n=9, P<0.06). LNAME did not affect the PG-induced reduction in IOP, and had no effect on IOP when used alone. Conclusions. After topical application of PGs in rabbits, the rise in IOP and aqueous protein levels are at least partially blocked by an NO synthase inhibitor, suggesting a possible role of endogenous NO.
|Original language||English (US)|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - Feb 15 1996|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience