Abstract
The intraocular pressure inside the human eye maintains 10-21 mmHg above the atmospheric pressure. Elevation of intraocular pressure is highly correlated with the retinopathy in glaucoma, and changes in the exterior pressure during mountain hiking, air traveling, and diving may also induce vision decline and retinopathy. The pathophysiological mechanism of these pressure-induced retinal disorders has not been completely clear. Retinal neurons express pressure-sensitive channels intrinsically sensitive to pressure and membrane stretch, such as the transient receptor potential channel (TRP) family permeable to Ca(2+) and Na(+) and the two-pore domain K channel family. Recent data have shown that pressure excites the primate retinal bipolar cell by opening TRP vanilloid 4 to mediate transient depolarizing currents, and TRP vanilloid 4 agonists enhance the membrane excitability of primate retinal ganglion cells. The eyeball wall is constructed primarily by the sclera and cornea of low elasticity, and the flow rate of the aqueous humor and intraocular pressure both fluctuate, but the mathematical relationship between the ocular elasticity, aqueous humor volume, and intraocular pressure has not been established. This review will briefly review recent literature on the pressure-related retinal pathophysiology in glaucoma and other pressure-induced retinal disorders, the elasticity of ocular tissues, and pressure-sensitive cation channels in retinal neurons. Emerging data support the global volume and the elasticity and thickness of the sclera and cornea as variables to affect the intraocular pressure level like the volume of the aqueous humor. Recent results also suggest some potential routes for TRPs to mediate retinal ganglion cell dysfunction: TRP opening upon intraocular pressure elevation and membrane stretch, enhancing glutamate release from bipolar cells, increasing intracellular Na(+), Ca(2+) concentration in retinal ganglion cells and extracellular glutamate concentration, inactivating voltage-gated Na(+) channels, and causing excitotoxicity and dysfunction of retinal ganglion cells. Further studies on these routes likely identify novel targets and therapeutic strategies for the treatment of pressure-induced retinal disorders.