Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo

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 ofl-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${}_2^{-}$ and NO${}_3^{-}$ (NO_x) or Glu levels by in vivo microdialysis before, during, and after infusion of NMDA in anesthetized rats. We also examined effects ofN^ω-nitro-l-arginine methyl ester (l-NAME) on the changes in these levels. NMDA elicited depressor and bradycardic responses and increased the levels of NO_x and Glu. l-NAME abolished the increases in the levels of NO_x 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.