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M. Shahidullah, M.K. Yap, C.–H. To; Nitric oxide donors reduce aqueous humor formation and IOP in the isolated arterially perfused pig eye . Invest. Ophthalmol. Vis. Sci. 2004;45(13):1033.
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Purpose: To investigate the effect of nitric oxide (NO) on aqueous humour formation (AHF) and intraocular pressure (IOP) of isolated pig eye using nitric oxide donors, sodium azide and sodium nitroprusside (SNP). Methods: Fresh pig eyes were cannulated through the ophthalmic artery and perfused with oxygenated Krebs' solution at 37°C. AHF and IOP were measured by fluorescein dilution technique and by direct cannulation of anterior chamber, respectively. We have studied the effect of NO donors, a physiological precursor of NO (L–arginine), and cGMP on AHF, IOP and uveal vasculature. Results: L–arginine (1.0mM), a physiological precursor of NO, but not D–arginine (1.0mM) the inactive analogue, produced a significant reduction in AHF (28.5%) and IOP (21.1 %). L–NAME (10 – 100µM), an inhibitor of NO synthase (NOS), had no effect on AHF and IOP. However, L–NAME (100µM) can completely block the IOP and AHF– lowering effect of L–arginine. Sodium azide and SNP produced concentration–dependent decrease in AHF and IOP. Sodium azide at concentrations of 100 nM, 1µM and 10 µM reduced AHF by 26.0, 39.7 and 51.7% and IOP by 10.8, 17.3 and 24.0%, respectively. SNP at 1µM, 10µM and 100µM reduced AHF by 6.0, 24.2 and 35.4% and IOP by 3.5, 9.5 and 15.5%, respectively. 8–pCPT–cGMP (10µM), a cell permeable analogue of cGMP, also reduced AHF (34.9%) and IOP (15.9%). The AHF and IOP–lowering effects of both sodium azide and SNP were blocked by ODQ (10µM), a specific inhibitor of soluble guanylate cyclase. However, ODQ (10µM) failed to block the AHF and IOP–lowering effect of 8–pCPT–cGMP. None of the drugs used had any significant effect on ocular arterial pressure. Conclusions:Nitric oxide donors, sodium azide and SNP, reduce AHF and IOP but had no effect on ocular vasculature. The reduction of AHF and IOP by nitrovasodilators is likely to involve the NO–cGMP pathway. NO may regulate AHF via mechanisms independent of ocular vasculature.
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