Neurogenic nitric oxide (NO) in the regulation of cerebroarterial tone

Sympathetic vasoconstrictor nerves are commonly recognized to mainly control the vascular smooth muscle tone, thus alters regional vascular resistance and blood flow. In contrast to peripheral organs and tissues, regulation by sympathetic nerves of blood flow in the brain is not so evident, and conversely vasodilator innervation is expected to play an important role. The mechanism underlying the neurogenic vasodilation in the cerebral artery has not been determined until recently. This problem was solved by the discovery of nitric oxide (NO) synthase inhibitors. Cerebral arterial dilatation caused by nerve stimulation is abolished by NO synthase inhibition and is restored by L-arginine, a substrate of NO synthase; vasodilator nerve stimulation increases the production of cyclic GMP in the tissue and liberates NOx (nitroxy compounds) from the arterial strip into superfusate. In addition, the presence of neurons containing NO synthase is histochemically demonstrated in the arterial wall. Neurogenic cerebral arterial dilation is thus hypothesized to be mediated by NO liberated as a neurotransmitter from the nerve. Nitroxidergic vasodilator innervation from the pterygopalatine ganglion would be important in the regulation of brain circulation.