Hirooka Kazuyuki, Shiraga Fumio
Department of Ophthalmology, Kagawa University Faculty of Medicine, Miki, Kagawa, Japan.
Clin Ophthalmol. 2007 Sep;1(3):217-23.
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.
针对缓解正常眼压性青光眼（NTG）基本病理过程的治疗方法尚未确立。尽管眼内压（IOP）在大多数患者中似乎无疑是一个危险因素，但降低眼压并不能阻止每一位NTG患者病情进展，这表明除眼压升高外的其他因素也参与了青光眼的病情进展。正在研究的新治疗途径包括可改善眼部血流的药物和神经保护药物。肾素-血管紧张素系统的主要成分已在眼组织中被鉴定出来。血管紧张素转换酶（ACE）抑制剂被广泛用于治疗全身性高血压。ACE抑制剂是激肽酶II的抑制剂，因此可防止缓激肽的分解。缓激肽通过培养的视网膜神经元中的缓激肽B（2）受体对谷氨酸神经毒性发挥保护作用。ACE抑制剂可阻止血管紧张素I转化为血管紧张素II。降低血管紧张素II水平可能通过减少血管超氧阴离子生成而对病情转归产生有益影响。ACE抑制剂作为一种潜在的抗青光眼治疗方法的效果值得深入研究。
