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 language | English (US) |
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Journal | American Journal of Physiology - Heart and Circulatory Physiology |
Volume | 266 |
Issue number | 5 35-5 |
State | Published - 1994 |
Keywords
- autonomic nervous system
- cats
- CP-96,345
- exercise
- groups III and IV muscle afferents
- spinal cord
ASJC Scopus subject areas
- Agricultural and Biological Sciences(all)
- Physiology