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

Isamu Matsuo, Yoshitaka Hirooka, Kiyoshi Hironaga, Kenichi Eshima, Hideaki Shigematsu, Miwako Shihara, Koji Sakai, Akira Takeshita

Research output: Contribution to journalArticlepeer-review

58 Citations (Scopus)

Abstract

Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo. Am J Physiol Regulatory Integrative Comp Physiol 280: R1285-R1291, 2001. - 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 NO2- and NO3- (NOx) or Glu levels by in vivo microdialysis before, during, and after infusion of NMDA in anesthetized rats. We also examined effects of Nω-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.

Original languageEnglish
Pages (from-to)R1285-R1291
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume280
Issue number5 49-5
DOIs
Publication statusPublished - May 2001

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

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