Noack E
Institut für Pharmakologie, Universität Düsseldorf, BRD.
Ophthalmologica. 1988;196(2):76-81. doi: 10.1159/000309879.
After 20 years of extensive practical experience in the management of glaucoma, beta-adrenergic blocking agents have gained a continuously increasing importance. The reason is a combination of effective reduction of intraocular pressure even during chronic treatment and few adverse effects. For many years, substantial effort has been focussed on the elucidation of the cellular mechanism inducing the intracellular pressure reduction. In this respect, mainly three different hypotheses have been controversially discussed: beta-blockers reduce aqueous humor formation (1) by an unspecific membrane-stabilizing process, (2) by impeding the local circulation of the ciliary body or (3) by specifically blocking adrenergic beta-receptors intimately involved in the regulation of aqueous humor production. Recently, substantial progress has been achieved by different working groups getting highly purified melanin-depleted fractions of ciliary epithelia which allow accurate receptor-ligand binding studies. The most important results, which all favor the explanation that the mechanism of action is due to specific inhibition of adrenergic receptors of the beta-2-subtype, are presented here. The consequences which result for the development of more specific pharmacologic agents in the future are discussed.
在青光眼治疗领域拥有20年丰富实践经验后，β-肾上腺素能阻滞剂的重要性持续攀升。原因在于其即便在长期治疗期间也能有效降低眼压，且副作用较少。多年来，大量工作致力于阐明导致眼压降低的细胞机制。在这方面，主要有三种不同假说引发了争议性讨论：β受体阻滞剂降低房水生成，（1）通过非特异性膜稳定过程，（2）通过阻碍睫状体局部循环，或（3）通过特异性阻断与房水生成调节密切相关的肾上腺素能β受体。最近，不同研究团队取得了重大进展，他们获得了高度纯化的无黑色素睫状体上皮细胞组分，这使得精确的受体-配体结合研究成为可能。本文呈现了最重要的结果，所有这些结果都支持作用机制是由于特异性抑制β2亚型肾上腺素能受体这一解释。文中还讨论了这一结果对未来开发更具特异性的药物制剂的影响。
