Calcium channels and their blockers in intraocular pressure and glaucoma

Several factors besides high intraocular pressure assumed to be associated with the development and progression of glaucoma, and calcium channel blockers (CCBs) have been an anticipated option for glaucoma treatment by improving ocular perfusion and/or exerting neuroprotective effects on retinal ganglion cells with safety established in wide and long-term usage. Decrease in IOP has been reported after topical application of CCBs, however, the effect is much smaller and almost negligible after systemic application. Various CCBs have been reported to increase posterior ocular blood flow in vivo and to exert direct neuroprotection in neurons in vitro. Distribution of the drug at a pharmacologically active concentration in the posterior ocular tissues across the blood–brain barrier or blood–retina barrier, especially in the optic nerve head and retina where the ganglion cells mainly suffer from glaucomatous damage, is essential for clinical treatment of glaucoma. Improved visual functions such as sensitivity in the visual field test have been reported after administration of CCBs, but evidences from the randomized studies have been limited and effects of CCBs on blood flow and direct neuroprotection are hardly distinguished from each other.