Hemodynamic regulatory mechanisms independent of metabolite
buildup or substrate depletion have been well demonstrated.
The microvasculature of the brain is highly responsive
to changes in the chemical composition of the
extracellular fluid (i.e., K+, Ca2", adenosine) that result from
shifts in neuronal membrane potentials (19-22). Of these, K+
is the most extensively studied and almost certainly plays a
major role in CBF regulation during both physiological and
pathological neuronal excitation. Neurogenic regulation of
local CBF also occurs, although the conditions under which
it is operative are not yet understood. The existence of
neuronal networks emanating from the basal forebrain and
the fastigial nucleus of the cerebellum that produce increases
in CBF without accompanying increases in metabolic rate has
been established by Reis and coworkers