LAUSR

A reduction in intraocular pressure (IOP) is the only recognized therapy for glaucoma. Hence, drugs exhibiting ocular hypotensive effects are important targets for antiglaucomatous drug development. IOP is determined by the equilibrium of aqueous humor production and outflow through either the trabecular meshwork or the uveoscleral outflow pathway. There is increasing evidence that nitric oxide (NO) has a major role in the regulation of IOP by directly acting on the trabecular meshwork and thereby lowering IOP. Taking advantage of this mechanism, newly designed NO-donating drugs combine the IOP-lowering effect of known substances with the trabecular meshwork outflow-increasing effect of NO. Here, we review the molecular mechanism of this new entity of IOP-lowering drugs.