Effect of Nitric Oxide (NO) synthase inhibition on the transient Intraocular Pressure (IOP) increase and Blood-Aqueous Barrier (BAB) breakdown after topically applied prostaglandins (PGs) in rabbits

G. L. Zhan, C. B. Camras, Carol B Toris, L. Tang

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Abstract

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. PGF (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 PGF 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 PGF, respectively, and inhibited by 57% the 9.3±2.1 mmHg rise after PGE2 (n=6). LNAME inhibited the PGF-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 languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number3
StatePublished - Feb 15 1996

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Blood-Aqueous Barrier
Intraocular Pressure
Nitric Oxide Synthase
Prostaglandins
Dinoprost
Rabbits
Dinoprostone
Nitric Oxide
Proteins
Aqueous Humor

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

@article{bfe86c48e2484dedb9b5608aa81b9bb8,
title = "Effect of Nitric Oxide (NO) synthase inhibition on the transient Intraocular Pressure (IOP) increase and Blood-Aqueous Barrier (BAB) breakdown after topically applied prostaglandins (PGs) in rabbits",
abstract = "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.",
author = "Zhan, {G. L.} and Camras, {C. B.} and Toris, {Carol B} and L. Tang",
year = "1996",
month = "2",
day = "15",
language = "English (US)",
volume = "37",
journal = "Investigative Ophthalmology and Visual Science",
issn = "0146-0404",
publisher = "Association for Research in Vision and Ophthalmology Inc.",
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TY - JOUR

T1 - Effect of Nitric Oxide (NO) synthase inhibition on the transient Intraocular Pressure (IOP) increase and Blood-Aqueous Barrier (BAB) breakdown after topically applied prostaglandins (PGs) in rabbits

AU - Zhan, G. L.

AU - Camras, C. B.

AU - Toris, Carol B

AU - Tang, L.

PY - 1996/2/15

Y1 - 1996/2/15

N2 - 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.

AB - 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.

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JO - Investigative Ophthalmology and Visual Science

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