Increasing evidence indicates that nitric oxide is an endogenous regulator of aqueous humor dynamics.1-7
The latest scientific evidence points to a role for nitric oxide depletion in the abnormal function of the primary aqueous outflow pathway.1,7,8
1. Aliancy J, Stamer WD, Wirostko B. A review of nitric oxide for the treatment of glaucomatous disease. Ophthalmol Ther. 2017;6(2):221-232. 2. Ellis DZ, Sharif NA, Dismuke WM. Endogenous regulation of human Schlemm’s canal cell volume by nitric oxide signaling. Invest Ophthalmol Vis Sci. 2010;51(11):5817-5824. 3. Stamer WD, Lei Y, Boussommier-Calleja A, Overby DR, Ethier CR. eNOS, a pressure-dependent regulator of intraocular pressure. Invest Ophthalmol Vis Sci. 2011;52(13):9438-9444. 4. Ashpole NE, Overby DR, Ethier CR, Stamer WD. Shear stress-triggered nitric oxide release from Schlemm’s canal cells. Invest Ophthalmol Vis Sci. 2014;55(12):8067-8076. 5. Lei Y, Zhang X, Song M, Wu J, Sun X. Aqueous humor outflow physiology in NOS3 knockout mice. Invest Ophthalmol Vis Sci. 2015;56(8):4891-4898. 6. McDonnell F, Perkumas KM, Ashpole NE, et al. Shear stress in Schlemm’s canal as a sensor of intraocular pressure. Sci Rep. 2020;10(1):5804. 7. Galassi F, Renieri G, Sodi A, Ucci F, Vannozzi L, Masini E. Nitric oxide proxies and ocular perfusion pressure in primary open angle glaucoma. Br J Ophthalmol. 2004;88(6):757-760. 8. Doganay S, Evereklioglu C, Turkoz Y, Er H. Decreased nitric oxide production in primary open-angle glaucoma. Eur J Ophthalmol. 2002;12(1):44-48.
