Therapeutic methods directed at alleviating the basic pathological processes of normal-tension glaucoma (NTG) are yet to be established. Although there seems to be little doubt that intraocular pressure (IOP) represents a risk factor in most patients, reduction of IOP does not prevent progression in every patient with NTG, indicating that factors other than elevated IOP are involved in glaucoma progression. New avenues of treatment under investigation include agents that could improve blood flow to the eye and neuroprotective drugs. The major components of the renin-angiotensin system have been identified in ocular tissue. Angiotensin-converting enzyme (ACE) inhibitors are widely used to treat systemic hypertension. ACE inhibitors are inhibitors of kininase II and thus prevent breakdown of bradykinin. Bradykinin displays protective actions against glutamate neurotoxicity through bradykinin-B(2) receptors in cultured retinal neurons. ACE inhibitors blocked the liberation of angiotensin II from angiotensin I. Lower angiotensin II levels may have beneficial effects on outcomes by lowering vascular superoxide anion production. The effects of ACE inhibitor as a potential antiglaucoma therapy deserve intense scrutiny.