TY - JOUR
T1 - Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo
AU - Matsuo, Isamu
AU - Hirooka, Yoshitaka
AU - Hironaga, Kiyoshi
AU - Eshima, Kenichi
AU - Shigematsu, Hideaki
AU - Shihara, Miwako
AU - Sakai, Koji
AU - Takeshita, Akira
PY - 2001/5
Y1 - 2001/5
N2 - 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.
AB - 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.
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U2 - 10.1152/ajpregu.2001.280.5.r1285
DO - 10.1152/ajpregu.2001.280.5.r1285
M3 - Article
C2 - 11294745
AN - SCOPUS:0035033976
SN - 0363-6119
VL - 280
SP - R1285-R1291
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 5 49-5
ER -