Blockade of non-NMDA receptors attenuates reflex pressor response to static contraction

J. M. Hill, J. G. Pickar, Marc Kaufman

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Considerable evidence suggests that both substance P and glutamate play a role in the spinal transmission of the exercise pressor reflex. We tested two hypotheses. First, after a lumbosacral intrathecal injection of a glutamatergic receptor antagonist, the reflex cardiovascular and ventilatory responses to static contraction are attenuated. Second, after a lumbosacral intrathecal injection of a substance P receptor antagonist and a glutamatergic receptor antagonist, the reflex cardiovascular and ventilatory responses to static contraction are abolished. We found that 1) the reflex cardiovascular responses to static contraction were unaffected (P > 0.05) after the intrathecal injection of the N-methyl-D-aspartate (NMDA) receptor antagonists, dl-2-amino-5-phosphonopentanoate (±AP-5) or 3-[(±)-2- carboxypiperazin-4-yl]propyl-1-phosphonic acid (±CPP); 2) the reflex pressor response to static muscular contraction was attenuated by >50% after the intrathecal injection of the non-NMDA receptor antagonist, 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX); and 3) the reflex pressor response to static contraction was almost abolished after the intrathecal injection of the substance P receptor antagonist, CP-96,345, and CNQX. Our results suggest that substance P and glutamate are two neurotransmitters involved in the spinal transmission of the exercise pressor reflex and that substance P and glutamate exert their effects via neurokinin-1 (NK-1) and non-NMDA receptors, respectively.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume266
Issue number5 35-5
StatePublished - Jan 1 1994

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D-Aspartic Acid
Spinal Injections
Reflex
Substance P
Neurokinin-1 Receptor Antagonists
Glutamic Acid
6-Cyano-7-nitroquinoxaline-2,3-dione
2-Amino-5-phosphonovalerate
Muscle Contraction
aspartic acid receptor
N-Methyl-D-Aspartate Receptors
Neurotransmitter Agents

All Science Journal Classification (ASJC) codes

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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title = "Blockade of non-NMDA receptors attenuates reflex pressor response to static contraction",
abstract = "Considerable evidence suggests that both substance P and glutamate play a role in the spinal transmission of the exercise pressor reflex. We tested two hypotheses. First, after a lumbosacral intrathecal injection of a glutamatergic receptor antagonist, the reflex cardiovascular and ventilatory responses to static contraction are attenuated. Second, after a lumbosacral intrathecal injection of a substance P receptor antagonist and a glutamatergic receptor antagonist, the reflex cardiovascular and ventilatory responses to static contraction are abolished. We found that 1) the reflex cardiovascular responses to static contraction were unaffected (P > 0.05) after the intrathecal injection of the N-methyl-D-aspartate (NMDA) receptor antagonists, dl-2-amino-5-phosphonopentanoate (±AP-5) or 3-[(±)-2- carboxypiperazin-4-yl]propyl-1-phosphonic acid (±CPP); 2) the reflex pressor response to static muscular contraction was attenuated by >50{\%} after the intrathecal injection of the non-NMDA receptor antagonist, 6-cyano-7- nitroquinoxaline-2,3-dione (CNQX); and 3) the reflex pressor response to static contraction was almost abolished after the intrathecal injection of the substance P receptor antagonist, CP-96,345, and CNQX. Our results suggest that substance P and glutamate are two neurotransmitters involved in the spinal transmission of the exercise pressor reflex and that substance P and glutamate exert their effects via neurokinin-1 (NK-1) and non-NMDA receptors, respectively.",
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Blockade of non-NMDA receptors attenuates reflex pressor response to static contraction. / Hill, J. M.; Pickar, J. G.; Kaufman, Marc.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 266, No. 5 35-5, 01.01.1994.

Research output: Contribution to journalArticle

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