advertisement
Nitric oxide (NO) plays an important role in retinal neurotransmission and in the regulation of blood flow. Expression of neuronal nitric oxide synthase (nNOS) in the retina is seen mainly in the internal retina, in cells such as the amacrine cells. NO is known to modulate light adaptation and receptive field size of the horizontal cells, but much remains to be clarified as to the retinal function of NO. Retinal guanylate cyclase (RetGC), which is involved in phototransduction, is not activated by NO, but is mediated by Ca2+. Impaired regulation of RetGC activities causes photoreceptor degeneration. Other than the regulation of basal current, NO may also play a role in the autoregulation of the circulation in the optic nerve head (ONH) during elevated IOP. However, in an ischemic condition, NO is inactivated by increased superoxide anion and changed into peroxynitrite, which has toxic effect on retinal tissue. To ensure successful clinical treatment for retinal ischemia, this paradoxical toxicity of NO needs to be addressed.LA: Japanese
H. Oku, MD, Department of Ophthalmology, Osaka Medical College, Osaka, Japan
1.3 Pathogenesis (Part of: 1 General aspects)