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Keywords
Abstract
The role of nitric oxide (NO), usually considered as a potent vasodilator, in regulating retinal neurovascular coupling is still elusive. Measurements of flicker light-induced functional hyperemia (FH) in humans show that an increase of NO levels reduces vasodilation. This evidence has led to conjecture that such an increase may be responsible for suppressing flicker-evoked vasodilation in diabetic retinopathy. In this paper, we propose a mathematical model to theoretically investigate the effect of an increase in neural NO (nNO) on the vasodilation of retinal arterioles. Simulation results indicate that nNO increase may:
1. significantly aff ect vasoconstrictive agent production by glial cells; and
2. elicit vasoconstriction rather than vasodilation in retinal arterioles.
Model predictions seem therefore to support the conjecture that NO increase may be responsible for suppressing flicker-evoked vasodilation in diabetic retinopathy.
References
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