Abstract
Pharmacological blockade of N-methyl- d-aspartic acid (NMDA) receptors in the spinal cord was produced by intrathecal administration of the NMDA receptor antagonist d-2-amino-7-phosphonoheptanoic acid. Blockade of spinal NMDA receptors significantly reduced arterial pressure, heart rate and sympathetic nerve activity and reduced by approximately 50% the pressor and sympathoexcitatory responses evoked by cerebral ischemia. These results indicate that NMDA receptors in the spinal cord participate in the maintenance and regulation of the sympathetic nervous system and suggest that excitatory amino acid neurotransmitters may play a role in sympathoexcitation produced by physiological activation of descending bulbospinal pathways.
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