Please use this identifier to cite or link to this item:
標題: Nitric oxide and glutamate in the dorsal facial area regulate common carotid blood flow in the cat
作者: Kuo, J.S.
Lee, T.J.F.
Chiu, Y.T.
Li, H.T.
Lin, N.N.
Tsai, T.T.
Gong, C.L.
關鍵字: carotid artery;medulla;cerebral blood flow;glutamatergic neuron;nitrergic neuron;parasympathetic nucleus;transmitter;rostral ventrolateral medulla;nucleus-tractus-solitarius;brain-stem;nervous-system;conscious rats;neurons;stimulation;mechanisms;receptors;microdialysis
Project: European Journal of Pharmacology
期刊/報告no:: European Journal of Pharmacology, Volume 594, Issue 1-3, Page(s) 55-63.
Nitric oxide (NO) or glutamate stimulation of dorsal facial area (DFA) increases blood flow in the common carotid artery (CCA), which supplies intra-and extra-cranial tissues. Nitrergic fibers and neurons as well as preganglionic cholinergic neurons are present in the DFA. We hypothesized the presence of nitrergic-glutamatergic fibers and preganglionic nitrergic-Cholinergic neurons in the DFA that are involved in the regulation of CCA blood flow. In microdialysis studies, perfusion of the DFA with S-nitroso-Nacetylpenicillamine (SNAP, an NO donor) increased the glutamate concentration in the dialysate. This effect was abolished by co-perfusion of methylene blue (a guanylyl cyclase inhibitor). Intra-DFA injection of L-arginine (an NO precursor) or glutamate increased CCA blood flow. The L-arginine-induced flow increase was reduced by prior administration of NG-nitro-arginine methyl ester (L-NAME, a non-specific NO synthase inhibitor), 7-nitroindazole (7-NI, a relatively selective neuronal NO synthase inhibitor), D-2amino-5-phosphonopentanoate (D-AP5, a competitive NMDA receptor antagonist), or glutamate diethylester (GDEE, a competitive AMPA receptor antagonist). The glutamate-induced blood flow increase was reduced by prior administration of L-NAME, 7-NI, or methylene blue. The induced increase in CCA blood flow, however, was not affected by endothelial NO synthase inhibitor. The findings indicate that NO-signal transduction within the DFA might cause glutamate release from presynaptic nitrergic-glutamatergic fibres and that the released glutamate activates NMDA/AMPA receptors on preganglionic nitrergic-cholinergic neurons in the nucleus to activate neuronal NO synthase and guanylyl cyclase in the neurons, leading to an increase in CCA blood flow. These findings may be important for developing therapeutic strategies for the diseases associated with CCA blood flow. (C) 2008 Elsevier B.V. All rights reserved.
ISSN: 0014-2999
DOI: 10.1016/j.ejphar.2008.07.020
Appears in Collections:期刊論文

Show full item record

Google ScholarTM




Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.