Aqueous Humor Formation and Its Regulation by Nitric Oxide: A Mini Review

C. Do, C. Kong, Chu‐yan Chan, Chuen Lam, C. To
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引用次数: 1

Abstract

Glaucoma is a common and severe aging eye disease which can cause permanent visual loss if untreated. One common strategy of glaucoma treatment is to lower the intraocular pressure (IOP) of the eye. So far, the pharmacologic reduction of IOP is the only proven intervention that can delay the progression of glaucomatous damage. Lowering the IOP can be achieved either by reducing the rate of aqueous humor secretion or by facilitating the rate of aqueous drainage. The formation of aqueous humor is driven primarily by vectorial ion transport, mainly Cl–, across the ciliary epithelium from ciliary stroma into the posterior chamber, resulting in the generation of an osmotic gradient which drives water movement. Many ion transporters and channels have been shown to participate in the process of aqueous secretion. Among several other signaling mechanisms, the nitric oxide (NO) signaling cascade is thought to regulate the ion transport across the ciliary epithelium, thereby reducing the rate of aqueous humor formation and IOP. Therefore, in this review, the potential significance of NO in the regulation of aqueous humor formation and IOP will be discussed.
一氧化氮对房水形成及其调控的研究进展
青光眼是一种常见且严重的老年性眼病,如果不治疗可导致永久性视力丧失。青光眼治疗的一个常见策略是降低眼内压(IOP)。到目前为止,药物降低IOP是唯一被证实可以延缓青光眼损害进展的干预措施。降低IOP可以通过降低房水分泌速率或促进房水排出速率来实现。房水的形成主要是由载体离子运输驱动的,主要是Cl -,从睫状体间质穿过睫状体上皮进入后房,导致渗透梯度的产生,从而驱动水的运动。许多离子转运体和通道已被证明参与水分泌过程。在其他几个信号传导机制中,一氧化氮(NO)信号级联被认为可以调节睫状体上皮的离子运输,从而降低房水形成速率和IOP。因此,本文将讨论一氧化氮在房水形成和IOP调节中的潜在意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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