Regular ArticleNitrovasodilator Effects on Intraocular Pressure and Outflow Facility in Monkeys
References (0)
Cited by (114)
Comparison of the Effects of Latanoprostene Bunod and Timolol on Retinal Blood Vessel Density: A Randomized Clinical Trial
2022, American Journal of OphthalmologyThe role of nitric oxide in ocular surface physiology and pathophysiology
2021, Ocular SurfaceThe vital role for nitric oxide in intraocular pressure homeostasis
2021, Progress in Retinal and Eye ResearchNitric oxide: a drug target for glaucoma revisited
2019, Drug Discovery TodayCitation Excerpt :Studies in nonhuman primates confirmed these results. As such, it was shown that the nitrovasodilators nitroglycerin and hydralazine decreased IOP in monkeys, an effect that was paralleled by a 92% increase in outflow facility [64]. However, the clinical use of nitrovasodilators is limited by the short half-life of NO in tissue, which makes it difficult to obtain sufficient drug concentrations at the level of the target tissue.
Carbonic anhydrase inhibitors as ophthalmologic drugs for the treatment of glaucoma
2019, Carbonic Anhydrases: Biochemistry and Pharmacology of an Evergreen Pharmaceutical TargetThe nitric oxide-guanylate cyclase pathway and glaucoma
2018, Nitric Oxide - Biology and ChemistryCitation Excerpt :In many cases, the effect of NO on IOP is linked to the action of its downstream messenger cGMP, particularly in the conventional outflow pathway (see Fig. 1). Stimulation of the NO-GC-1-cGMP pathway via administration of NO donor compounds lowers IOP through relaxation of the TM, alteration of TM volume, and an increase in the permeability of cells in the SC [76,120–127]. In addition, increased iNOS is observed following increased perfusion pressure in the anterior segments of human donor eyes [128].