Respiratory modulation of sympathetic nerve activity: Effect of MK-801

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Abstract

The modulation of splanchnic sympathetic nerve activity (SNA) by brain stem neural networks generating the respiratory rhythm was examined in decerebrate, unanesthetized, vagotomized, artificially ventilated rats before and after blockade of the N-methyl-D-aspartate (NMDA) channel with intravenous administration of dizocilpine (MK-801). NMDA channel blockade 1) prolonged inspiration and reduced the phrenic nerve amplitude, 2) reduced SNA to 40% of control levels, and 3) decreased mean arterial pressure by 20 mmHg. A strong synchronization of SNA to the central respiratory cycle (monitored by the activity on the phrenic nerve) was maintained after MK-801 administration, although a brief inhibition of SNA during early inspiration and a sympathetic excitation during early expiration were eliminated. These results suggest 1) the existence of an NMDA-independent mechanism by which some elements of the brain stem respiratory network excite sympathetic outflow, 2) that the NMDA-mediated influence of specific classes of brain stem respiratory neurons can modulate this excitation during portions of the respiratory cycle, and 3) that an NMDA-dependent excitation in the brain stem or spinal cord plays a significant role in maintaining basal levels of splanchnic SNA.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume270
Issue number3 39-3
StatePublished - 1996
Externally publishedYes

Fingerprint

Dizocilpine Maleate
N-Methylaspartate
Brain Stem
Splanchnic Nerves
Phrenic Nerve
Activity Cycles
Intravenous Administration
Spinal Cord
Arterial Pressure
Neurons

Keywords

  • glutamate
  • N-methyl-D-aspartate receptors
  • phrenic nerve
  • splanchnic nerve

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Cite this

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title = "Respiratory modulation of sympathetic nerve activity: Effect of MK-801",
abstract = "The modulation of splanchnic sympathetic nerve activity (SNA) by brain stem neural networks generating the respiratory rhythm was examined in decerebrate, unanesthetized, vagotomized, artificially ventilated rats before and after blockade of the N-methyl-D-aspartate (NMDA) channel with intravenous administration of dizocilpine (MK-801). NMDA channel blockade 1) prolonged inspiration and reduced the phrenic nerve amplitude, 2) reduced SNA to 40{\%} of control levels, and 3) decreased mean arterial pressure by 20 mmHg. A strong synchronization of SNA to the central respiratory cycle (monitored by the activity on the phrenic nerve) was maintained after MK-801 administration, although a brief inhibition of SNA during early inspiration and a sympathetic excitation during early expiration were eliminated. These results suggest 1) the existence of an NMDA-independent mechanism by which some elements of the brain stem respiratory network excite sympathetic outflow, 2) that the NMDA-mediated influence of specific classes of brain stem respiratory neurons can modulate this excitation during portions of the respiratory cycle, and 3) that an NMDA-dependent excitation in the brain stem or spinal cord plays a significant role in maintaining basal levels of splanchnic SNA.",
keywords = "glutamate, N-methyl-D-aspartate receptors, phrenic nerve, splanchnic nerve",
author = "Shaun Morrison",
year = "1996",
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AU - Morrison, Shaun

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N2 - The modulation of splanchnic sympathetic nerve activity (SNA) by brain stem neural networks generating the respiratory rhythm was examined in decerebrate, unanesthetized, vagotomized, artificially ventilated rats before and after blockade of the N-methyl-D-aspartate (NMDA) channel with intravenous administration of dizocilpine (MK-801). NMDA channel blockade 1) prolonged inspiration and reduced the phrenic nerve amplitude, 2) reduced SNA to 40% of control levels, and 3) decreased mean arterial pressure by 20 mmHg. A strong synchronization of SNA to the central respiratory cycle (monitored by the activity on the phrenic nerve) was maintained after MK-801 administration, although a brief inhibition of SNA during early inspiration and a sympathetic excitation during early expiration were eliminated. These results suggest 1) the existence of an NMDA-independent mechanism by which some elements of the brain stem respiratory network excite sympathetic outflow, 2) that the NMDA-mediated influence of specific classes of brain stem respiratory neurons can modulate this excitation during portions of the respiratory cycle, and 3) that an NMDA-dependent excitation in the brain stem or spinal cord plays a significant role in maintaining basal levels of splanchnic SNA.

AB - The modulation of splanchnic sympathetic nerve activity (SNA) by brain stem neural networks generating the respiratory rhythm was examined in decerebrate, unanesthetized, vagotomized, artificially ventilated rats before and after blockade of the N-methyl-D-aspartate (NMDA) channel with intravenous administration of dizocilpine (MK-801). NMDA channel blockade 1) prolonged inspiration and reduced the phrenic nerve amplitude, 2) reduced SNA to 40% of control levels, and 3) decreased mean arterial pressure by 20 mmHg. A strong synchronization of SNA to the central respiratory cycle (monitored by the activity on the phrenic nerve) was maintained after MK-801 administration, although a brief inhibition of SNA during early inspiration and a sympathetic excitation during early expiration were eliminated. These results suggest 1) the existence of an NMDA-independent mechanism by which some elements of the brain stem respiratory network excite sympathetic outflow, 2) that the NMDA-mediated influence of specific classes of brain stem respiratory neurons can modulate this excitation during portions of the respiratory cycle, and 3) that an NMDA-dependent excitation in the brain stem or spinal cord plays a significant role in maintaining basal levels of splanchnic SNA.

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KW - N-methyl-D-aspartate receptors

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KW - splanchnic nerve

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