Examination of the role of nitric oxide for the hypercapnic rise of cerebral blood flow in rats

Nitric oxide synthase (NOS) inhibition through N(G)-nitro-L-arginine (L-NNA) TTX modulates the increase of cerebral blood flow in cerebellar cortex and parietal cortex in response to hypercapnia. The NOS, L-NNA inhibitor stimulates action when transported in blood than when topically applied. TTX suppresses perivascular nerve function near the cortical and pial vessels.