Glaucoma is a progressive optic neuropathy, characterized by loss of retinal ganglion cells with subsequent deterioration in visual field. A major clinically modifiable risk factor for glaucomatous deterioration is elevated intraocular pressure (IOP) as a sequence of an increased aqueous humor (AH) outflow resistance. Aside from the introduction of prostaglandin analogs, topical carbonic anhydrase inhibitors , and topical alpha agonists in the 1990s, a new pharmaceutical agents to lower IOP have been introduced approximately 20 years.
Rho-kinase (ROCK) Inhibitors, a new pharmacological class of hypotensive glaucoma medication targeting specifically the diseased trabecular outflow pathway. Rock inhibitors function by relaxing the trabecular meshwork, which subsequently leads to improved aqueous humor outflow and lower IOP. ROCK is a downstream effector of a small-G protein Rho.
In addition to improving the outflow facility of the trabecular meshwork, Rho kinase inhibitors also enhance retinal ganglion cell survival after ischemic injury and increase ocular blood flow. ROCK inhibitors were reported to block TGF-B myofibroblast differentiation of human tendon fibroblasts, suggesting that may reduce postoperative conjunctival scarring after glaucoma surgery
The objectives of this review are to describe the basic science underlying the mechanism of ROCK inhibitors as a therapy to lower IOP ,their neuro-protective, and vasoactive properties .