Neurovascular coupling describes a series of processes that serve to match blood supply to neuronal metabolism within the central nervous system. Non-human research has been clear in identifying the dilatory molecule nitric oxide as a primary contributor to the neurovascular coupling mechanism. These studies have shown that of the three nitric-oxide synthase enzymes that produce nitric oxide, the neuronal isoform (nNOS) is a primary contributor to neurovascular coupling. Although extremely important to reveal mechanisms, non-human neurovascular coupling research is often conducted with the use of potentially confounding vasoactive anaesthetics, restraint, and/or by using isolated preparations which lack flow-induced vascular tone, and key inputs such as that of the autonomic nervous system. Furthering our understanding of neurovascular coupling in humans can provide a greater mechanistic understanding by obviating these concerns, and may provide insight into cerebrovascular diseases where this process is impaired.The primary objective of this project was to test the role of nNOS in neurovascular coupling, using our established non-anaesthetized, non-stressed, human model. A secondary objective was to test the role of nNOS in cerebral autoregulation, which describes cerebral blood flow buffering against changes in systemic pressure. In healthy human participants, we continuously administered s-methyl-L-thiocitrulline (SMTC) intravenously to inhibit nNOS, while measuring beat-by-beat blood pressure end-tidal oxygen/carbon dioxide, and cerebral blood velocity in the posterior and middle cerebral arteries. Cerebral autoregulation measurements were obtained during a steady-state resting condition, and neurovascular coupling was elicited using a standardized visual stimulus. As SMTC leads to an increase in blood pressure, we matched the pressor effect of this drug using intravenous administration of phenylephrine. Neurovascular coupling was also assessed in participants using a placebo condition. Order of trials were randomized and completed in a double-blind fashion.As shown in the prepared manuscript included in this thesis, SMTC blunted the rapidity of the initial neurovascular coupling response to visual stimulus, compared to a matched pressor effect from phenylephrine. Furthermore, measurement of dynamic cerebral autoregulation showed impairment, particularly in the temporal response. These findings provide novel insight into the role of nNOS in the regulation of cerebral blood flow mechanisms in humans.