Glutamate stimulation of the dorsal facial area (DFA), an area located just dorsal to the facial area, produces increase in the blood flow of ipsilateral common carotid artery (CCA). Nitric oxide (NO) acts as a neurotransmitter and is closely related with glutamate in central nervous system. Whether NO might interact with glutamate to affect CCA blood flow was not known. Perfusion in the DFA of S-nitroso-N-acetylpenicillamine, a NO donor, increased glutamate concentration in the DFA and elicited CCA blood flow increase. Microinjection of sodium nitroprusside (NO donor) in the DFA caused dose-dependent increase in CCA blood flow. Microinjections of L-arginine (NO precursor) in the DFA also caused dose-dependent increase in CCA blood flow, suggesting NO synthesis in the DFA. Microinjection in the DFA of NG-nitro-arginine methyl ester (L-NAME, a NOS inhibitor) or methylene blue (guanylate cyclase inhibitor) caused a decrease in CCA blood flow, suggesting a tonic release of NO. Cells (probably neurons) containing NO synthase (NOS) were found in the DFA as approached by histochemical staining of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), a maker of NOS. In conclusion, NOS-containg cells or neurons are present in the DFA, and appear to release NO in tonic fashion and to interact with glutamate for increasing CCA blood flow. The result may provide some help in developing therapeutic strategy for CCA vascular disorders.
