CHANGES in nitric oxide (NO) concentration and cerebral blood flow (CB
F) in the parietal cortex during hypercapnoea were investigated in ana
esthetized rats, using a NO-selective electrode and laser Doppler flow
metry. When hypercapnoea was induced by inhalation of 5% CO2 for 10 mi
n, both the NO concentration and CBF increased. After administration o
f 7-nitroindazole, a neuronal NO synthase (nNOS) inhibitor, both the b
asal NO and CBF decreased, and responses to hypercapnoea were also sig
nificantly suppressed by 70.1% and 73.2%, respectively, compared with
the control state. These results suggest that NO derived from nNOS is
involved not only in maintaining resting cerebral circulation but also
in regulating CBF response during hypercapnoea.