The brain has high energetic and metabolic demands, which requires a precise communication between neuronal cells and the blood vessels. Neurovascular coupling (NYC) allows the allocation of resources to areas of higher energetic requirement with temporal and regional precision. One key mediator of NYC is nitric oxide ( • NO) produced in activated neurons by nNOS. Enzymatic production of • NO can be impaired in conditions like hypoxia, ageing and neurodegenerative diseases, impacting NYC. We hypothesize that low-level changes in basal • NO levels can result from modulation of circulating nitrite levels via dietary intervention with nitrate-rich foods, improving cerebrovascular function and NYC in aging and degeneration or stroke. In this work, we used gas phase chemiluminescence to quantify nitrite reduction between pH 6.0–7.4 in the presence of ascorbate, the more abundant reducing agent found in the brain extracellular space and released from neurons upon glutamatergic stimulation. Results support nitrite reduction to • NO by ascorbate as a function of pH. In vivo studies to assess the impact of nitrite-driven • NO in the functionality of NYC were implemented and preliminary data support a contribution of this mechanism to the maintenance of NYC.