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 journalArticle

57 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
Publication statusPublished - May 1 2001

Fingerprint

Solitary Nucleus
Bradycardia
Aspartic Acid
Hypotension
Glutamic Acid
Nitric Oxide
NG-Nitroarginine Methyl Ester
Microdialysis

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Matsuo, I., Hirooka, Y., Hironaga, K., Eshima, K., Shigematsu, H., Shihara, M., ... Takeshita, A. (2001). Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo. American Journal of Physiology - Regulatory Integrative and Comparative Physiology, 280(5 49-5), R1285-R1291.

Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo. / Matsuo, Isamu; Hirooka, Yoshitaka; Hironaga, Kiyoshi; Eshima, Kenichi; Shigematsu, Hideaki; Shihara, Miwako; Sakai, Koji; Takeshita, Akira.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 280, No. 5 49-5, 01.05.2001, p. R1285-R1291.

Research output: Contribution to journalArticle

Matsuo, I, Hirooka, Y, Hironaga, K, Eshima, K, Shigematsu, H, Shihara, M, Sakai, K & Takeshita, A 2001, 'Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo', American Journal of Physiology - Regulatory Integrative and Comparative Physiology, vol. 280, no. 5 49-5, pp. R1285-R1291.
Matsuo, Isamu ; Hirooka, Yoshitaka ; Hironaga, Kiyoshi ; Eshima, Kenichi ; Shigematsu, Hideaki ; Shihara, Miwako ; Sakai, Koji ; Takeshita, Akira. / Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2001 ; Vol. 280, No. 5 49-5. pp. R1285-R1291.
@article{4cb9d4c8f94a4bd48bba40597936204d,
title = "Glutamate release via NO production evoked by NMDA in the NTS enhances hypotension and bradycardia in vivo",
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.",
author = "Isamu Matsuo and Yoshitaka Hirooka and Kiyoshi Hironaga and Kenichi Eshima and Hideaki Shigematsu and Miwako Shihara and Koji Sakai and Akira Takeshita",
year = "2001",
month = "5",
day = "1",
language = "English",
volume = "280",
pages = "R1285--R1291",
journal = "American Journal of Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "5 49-5",

}

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 - 2001/5/1

Y1 - 2001/5/1

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.

UR - http://www.scopus.com/inward/record.url?scp=0035033976&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0035033976&partnerID=8YFLogxK

M3 - Article

C2 - 11294745

AN - SCOPUS:0035033976

VL - 280

SP - R1285-R1291

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6119

IS - 5 49-5

ER -