Nitric oxide and glutamate in the dorsal facial area regulate common carotid blood flow in the cat

Neurochemicals Involved in Medullary Control of Common Carotid Blood Flow

“…Neuronal release of glutamate is further confirmed by the findings that CCA blood flow increase induced by intra-DFA administrations of several neurochemicals, such as arginine (NO precursor), S-nitroso-N-acetylpenicillamine (NO donor) [18], ATP (P2 receptor agonist) [19], and choline (α7-nAChR agonist) or nicotine (non-specific nAChR agonist), can be inhibited by glutamatergic receptor antagonists. Furthermore, endo-genously released [18] and exogenously administered glutamate [13] are similarly blocked by the NMDA or AMPA receptor antagonist; both receptors have therefore been proposed to be present on preganglionic neurons, nitrergic and/or cholinergic neurons which give rise to the parasympathetic 7 th and 9 th preganglionic nerves [18]. …”

“…These findings suggest that activation by nicotine or choline of nACh receptors, primarily α7-nACh receptors, causes a release of glutamate, but does not cause a release of cholinergic substance that stimulates α7-nACh receptors in the DFA. The α7-nAChR and other nAChRs may be present on the nitrergic and/or glutamatergic fiber which innervates and releases glutamate to stimulate preganglionic neurons of the parasympathetic 7 th and 9 th cranial nerves, leading to an increase in CCA blood flow [18]. …”

“…The latter notion is seldom addressed except for a report in which presynaptic nitrergic and/or glutamatergic fibers have been proposed to be present in the solitary nucleus, releasing NO and glutamate in the regulation of sympathetic out flow [49]. Similar presynaptic nitrergic and/or glutamatergic fibers have been proposed to be present in the DFA in the regulation of CCA blood flow [18, 50] according to the following findings.…”

“…The increased CCA blood flow induced by intra-DFA administration of L-arginine is markedly inhibited not only by pretreatment with nNOS inhibitor but also by glutamate receptor antagonists, suggesting that nNOS-containing neurons/fibers may release glutamate in the DFA [50]. In microdialysis and HPLC studies, perfusion with a NO donor into the DFA increases, but co-perfusion of a NO donor with a guanylyl cyclase (GC) inhibitor blocks release of glutamate, further suggesting that glutamate is released from the nNOS/GC/cGMP-containing neuron/fiber in the DFA and glutamate release is triggered by cGMP [18]. The above findings suggest that the presynaptic glutamatergic fiber in the DFA can release glutamate through activation of the nNOS/GC/cGMP pathway in the fiber, and is defined as presynaptic nitrergic and/or glutamatergic fibers.…”

“…In conclusion, the presynaptic nitrergic and/or glutamatergic fibers that can release glutamate through activation of the nNOS/GC/cGMP in the fiber exist in the DFA for regulation of CCA blood flow [18]. …”