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Department of Cardiovascular Medicine, Cardiovascular Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan
Nitric oxide (NO) in the
nucleus tractus solitarii (NTS) plays an important role in regulating
sympathetic nerve activity. The aims of this study were to determine
whether the activation of N-methyl-D-aspartate
(NMDA) receptors in the NTS facilitates the release of
L-glutamate (Glu) via NO production, and, if so, to
determine whether this mechanism is involved in the depressor and
bradycardic responses evoked by NMDA. We measured the production of NO
in the NTS as NO

-nitro-L-arginine methyl ester
(L-NAME) on the changes in these levels. NMDA elicited
depressor and bradycardic responses and increased the levels of
NOx and Glu. L-NAME abolished the increases in
the levels of NOx and Glu and attenuated cardiovascular
responses evoked by NMDA. These results suggest that NMDA receptor
activation in the NTS induces Glu release through NO synthesis and that
Glu released via NO enhances depressor and bradycardic responses.
nitric oxide synthase; central nervous system; blood pressure; amino acid; microdialysis; nucleus tractus solitarii; N-methyl-D-aspartate
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