Aqueous humor formation and its regulation by nitric oxide: A mini review

Glaucoma is a common and severe aging eye disease which can cause permanent visual loss if untreated. One common strategy of glaucoma treatment is to lower the intraocular pressure (IOP) of the eye. So far, the pharmacologic reduction of IOP is the only proven intervention that can delay the progression of glaucomatous damage. Lowering the IOP can be achieved either by reducing the rate of aqueous humor secretion or by facilitating the rate of aqueous drainage. The formation of aqueous humor is driven primarily by vectorial ion transport, mainly Cl-, across the ciliary epithelium from ciliary stroma into the posterior chamber, resulting in the generation of an osmotic gradient which drives water movement. Many ion transporters and channels have been shown to participate in the process of aqueous secretion. Among several other signaling mechanisms, the nitric oxide (NO) signaling cascade is thought to regulate the ion transport across the ciliary epithelium, thereby reducing the rate of aqueous humor formation and IOP. Therefore, in this review, the potential significance of NO in the regulation of aqueous humor formation and IOP will be discussed.