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ennio ongini, Elena Bastia, Francesco Impagnatiello; Intraocular pressure and cGMP aqueous humor levels in spontaneous ocular hypertensive rabbits and following transient IOP changes. Invest. Ophthalmol. Vis. Sci. 2013;54(15):426.
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Molecular mechanisms underlying intraocular pressure (IOP) homeostasis are still unclear. There is emerging evidence that nitric oxide (NO) and the cGMP pathway are involved in the regulation of IOP. We studied NO - cGMP signaling and ocular tone in experimental models of glaucoma and following pharmacological modulation of intraocular pressure.
New Zealand White (NZW) and spontaneously ocular hypertensive Dutch Belted (DB) rabbits were used. Transient IOP raise was induced in NZW rabbits by the injection of 100μL hypertonic saline (5%) into the vitreous. cGMP levels were measured in aqueous humor (AH). IOP was monitored using a pneumatonometer prior to drug administration and at different time points thereafter.
Spontaneous ocular hypertensive DB rabbits had constant higher IOP and lower cGMP levels than normotensive NZW rabbits (IOP, 32±1.2 and 20±0.9mmHg, respectively p< 0.05; cGMP, 5.6±0.4 and 21.9±1.2 pmol/ml, respectively p<0.05).Transient raise in IOP in normotensive NZW rabbits (Tmax=15-60 min Δmax= 35.1±1.2 mmHg) following hypertonic saline resulted in concomitant decrease in AH cGMP levels (Tmax=60 min; Emax= 37%). Finally, in normotensive NZW rabbits, topical instillation of the IOP-lowering drug, timolol (1%) or the NO donors, S-Nitroso-N-Acetyl-D,L-Penicillamine (SNAP, 0.2%) and isosorbide-5-mononitrate (ISMN, 1%) decreased IOP (Δmax= -3.4±0.4, -2.4±0.4 and -2.2±0.4 mmHg, respectively p< 0.05 vs vehicle treated eyes) and concomitantly raised cGMP content in AH of treated eyes.
Data support the notion that the NO/cGMP signaling pathway is involved in the regulation of IOP.
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