Cardiovascular response to group I metabotropic glutamate receptor activation in NTS

C. Michael Foley, Helen W. Vogl, Patrick J. Mueller, Meredith Hay, Eileen M. Hasser

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Glutamate is the proposed neurotransmitter of baroreceptor afferents at the level of the nucleus tractus solitarius (NTS). Exogenous glutamate in the NTS activates neurons through ionotropic and metabotropic glutamate receptors (mGluRs). This study tested the hypothesis that group I mGluRs in the NTS produce depressor, bradycardic, and sympathoinhibitory responses. In urethan- anesthetized rats, unilateral 30-nl microinjections of the group I-selective mGluR agonist 3,5-dihydroxyphenylglycine (DHPG) into the NTS decreased mean arterial pressure, heart rate, and lumbar sympathetic nerve activity. The dose of drug that produced 50% of the maximal response (ED50) was 50-100 μM. The response to microinjection of equal concentrations of DHPG or the general mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (ACPD) produced similar cardiovascular effects. The cardiovascular response to injection of DHPG or ACPD was abolished by NTS blockade of mGluRs with α- methyl-4-carboxyphenylglycine (MCPG). Blockade of ionotropic glutamate receptors with kynurenic acid did not attenuate the response to DHPG or ACPD injection. These data suggest that DHPG and ACPD activate mGluRs in the NTS and do not require ionotropic glutamate receptors to produce their cardiovascular response. In the NTS the group I mGluRs produce responses that are consistent with excitation of neurons involved in reducing sympathetic outflow, heart rate, and arterial pressure.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume276
Issue number5 45-5
StatePublished - May 1999
Externally publishedYes

Fingerprint

Metabotropic Glutamate Receptors
Solitary Nucleus
Dicarboxylic Acids
Ionotropic Glutamate Receptors
Microinjections
Glutamic Acid
Arterial Pressure
Heart Rate
Kynurenic Acid
Neurons
Pressoreceptors
Injections
Urethane
Neurotransmitter Agents
dihydroxyphenylethylene glycol
Pharmaceutical Preparations

Keywords

  • 1-aminocyclopentane-1S
  • 3,5- dihydroxyphenylglycine
  • 3R-dicarboxylic acid
  • Arterial baroreflex
  • Sympathetic nerve activity

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

Cardiovascular response to group I metabotropic glutamate receptor activation in NTS. / Foley, C. Michael; Vogl, Helen W.; Mueller, Patrick J.; Hay, Meredith; Hasser, Eileen M.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 276, No. 5 45-5, 05.1999.

Research output: Contribution to journalArticle

@article{09d22783f5674b8abbc735608fdbb685,
title = "Cardiovascular response to group I metabotropic glutamate receptor activation in NTS",
abstract = "Glutamate is the proposed neurotransmitter of baroreceptor afferents at the level of the nucleus tractus solitarius (NTS). Exogenous glutamate in the NTS activates neurons through ionotropic and metabotropic glutamate receptors (mGluRs). This study tested the hypothesis that group I mGluRs in the NTS produce depressor, bradycardic, and sympathoinhibitory responses. In urethan- anesthetized rats, unilateral 30-nl microinjections of the group I-selective mGluR agonist 3,5-dihydroxyphenylglycine (DHPG) into the NTS decreased mean arterial pressure, heart rate, and lumbar sympathetic nerve activity. The dose of drug that produced 50{\%} of the maximal response (ED50) was 50-100 μM. The response to microinjection of equal concentrations of DHPG or the general mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (ACPD) produced similar cardiovascular effects. The cardiovascular response to injection of DHPG or ACPD was abolished by NTS blockade of mGluRs with α- methyl-4-carboxyphenylglycine (MCPG). Blockade of ionotropic glutamate receptors with kynurenic acid did not attenuate the response to DHPG or ACPD injection. These data suggest that DHPG and ACPD activate mGluRs in the NTS and do not require ionotropic glutamate receptors to produce their cardiovascular response. In the NTS the group I mGluRs produce responses that are consistent with excitation of neurons involved in reducing sympathetic outflow, heart rate, and arterial pressure.",
keywords = "1-aminocyclopentane-1S, 3,5- dihydroxyphenylglycine, 3R-dicarboxylic acid, Arterial baroreflex, Sympathetic nerve activity",
author = "Foley, {C. Michael} and Vogl, {Helen W.} and Mueller, {Patrick J.} and Meredith Hay and Hasser, {Eileen M.}",
year = "1999",
month = "5",
language = "English (US)",
volume = "276",
journal = "American Journal of Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "5 45-5",

}

TY - JOUR

T1 - Cardiovascular response to group I metabotropic glutamate receptor activation in NTS

AU - Foley, C. Michael

AU - Vogl, Helen W.

AU - Mueller, Patrick J.

AU - Hay, Meredith

AU - Hasser, Eileen M.

PY - 1999/5

Y1 - 1999/5

N2 - Glutamate is the proposed neurotransmitter of baroreceptor afferents at the level of the nucleus tractus solitarius (NTS). Exogenous glutamate in the NTS activates neurons through ionotropic and metabotropic glutamate receptors (mGluRs). This study tested the hypothesis that group I mGluRs in the NTS produce depressor, bradycardic, and sympathoinhibitory responses. In urethan- anesthetized rats, unilateral 30-nl microinjections of the group I-selective mGluR agonist 3,5-dihydroxyphenylglycine (DHPG) into the NTS decreased mean arterial pressure, heart rate, and lumbar sympathetic nerve activity. The dose of drug that produced 50% of the maximal response (ED50) was 50-100 μM. The response to microinjection of equal concentrations of DHPG or the general mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (ACPD) produced similar cardiovascular effects. The cardiovascular response to injection of DHPG or ACPD was abolished by NTS blockade of mGluRs with α- methyl-4-carboxyphenylglycine (MCPG). Blockade of ionotropic glutamate receptors with kynurenic acid did not attenuate the response to DHPG or ACPD injection. These data suggest that DHPG and ACPD activate mGluRs in the NTS and do not require ionotropic glutamate receptors to produce their cardiovascular response. In the NTS the group I mGluRs produce responses that are consistent with excitation of neurons involved in reducing sympathetic outflow, heart rate, and arterial pressure.

AB - Glutamate is the proposed neurotransmitter of baroreceptor afferents at the level of the nucleus tractus solitarius (NTS). Exogenous glutamate in the NTS activates neurons through ionotropic and metabotropic glutamate receptors (mGluRs). This study tested the hypothesis that group I mGluRs in the NTS produce depressor, bradycardic, and sympathoinhibitory responses. In urethan- anesthetized rats, unilateral 30-nl microinjections of the group I-selective mGluR agonist 3,5-dihydroxyphenylglycine (DHPG) into the NTS decreased mean arterial pressure, heart rate, and lumbar sympathetic nerve activity. The dose of drug that produced 50% of the maximal response (ED50) was 50-100 μM. The response to microinjection of equal concentrations of DHPG or the general mGluR agonist 1-aminocyclopentane-1S,3R-dicarboxylic acid (ACPD) produced similar cardiovascular effects. The cardiovascular response to injection of DHPG or ACPD was abolished by NTS blockade of mGluRs with α- methyl-4-carboxyphenylglycine (MCPG). Blockade of ionotropic glutamate receptors with kynurenic acid did not attenuate the response to DHPG or ACPD injection. These data suggest that DHPG and ACPD activate mGluRs in the NTS and do not require ionotropic glutamate receptors to produce their cardiovascular response. In the NTS the group I mGluRs produce responses that are consistent with excitation of neurons involved in reducing sympathetic outflow, heart rate, and arterial pressure.

KW - 1-aminocyclopentane-1S

KW - 3,5- dihydroxyphenylglycine

KW - 3R-dicarboxylic acid

KW - Arterial baroreflex

KW - Sympathetic nerve activity

UR - http://www.scopus.com/inward/record.url?scp=0032967171&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032967171&partnerID=8YFLogxK

M3 - Article

C2 - 10233041

AN - SCOPUS:0032967171

VL - 276

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6143

IS - 5 45-5

ER -