The role of nitric oxide in the cerebrovascular flow response to stimulation of postganglionic parasympathetic nerves in the rat.

Stimulation of cerebrovascular parasympathetic nerves markedly increases cortical blood flow. Nitric oxide (NO) or a NO containing compound is present in these nerves, and its release may therefore be partly responsible for the flow increase. In addition, transmitters released from the nerves may cause synthesis and release of this compound from the endothelium. The contribution of NO synthesis to the cortical blood flow increase during parasympathetic stimulation was elucidated in rats by laser-Doppler flowmetry. Thirty min exposure to circulating N omega-nitro-L-arginine methyl ester (L-NAME) 50 mg.kg-1 eliminated most of the response (from 104 to 8% increase), whereas 10 min exposure to this dose or 30 min exposure to 5 mg.kg-1 caused a less marked reduction. The reducing effect was particularly evident after elimination of the systemic blood pressure increase caused by L-NAME (only 3% increase after the high dose). In fusion of L-arginine restored the flow response. Resting cortical blood flow was not substantially affected by blockade of NO formation. Thus, release of a NO containing compound constitutes a major component of the increase in cortical blood flow caused by parasympathetic nerve stimulation, but does not seem to contribute to cortical flow regulation during resting conditions.