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Department of Medicine, University of California, Irvine, California 92697-4075
Abdominal ischemia induces a
pressor reflex caused mainly by C-fiber afferent stimulation. Because
excitatory amino acids, such as glutamate, bind to
N-methyl-D-aspartate (NMDA) and non-NMDA [dl-
-amino-3-hydroxy-5-methylisoxazole-4-propionate
(AMPA)] receptors and serve as important spinal neurotransmitters, we
hypothesized that both receptors play a role in the abdominal
ischemia pressor reflex. In chloralose-anesthetized cats, NMDA
receptor blockade with 25.0 mM
dl-2-amino-5-phosphonopentanoate did not alter the pressor
reflex (33 ± 9 to 33 ± 7 mmHg, P > 0.05, n = 4), whereas AMPA receptor blockade with 4.0 mM
6-nitro-7-sulfamylbenzo(f)quinoxaline-2,3-dione significantly attenuated the reflex (29 ± 5 to 16 ± 4 mmHg,
P < 0.05, n = 6). Because several studies
suggest that anesthesia masks the effects of glutamatergic receptors,
this experiment was repeated on decerebrate cats, and in this group,
NMDA receptor blockade with 25.0 mM
dl-2-amino-5-phosphonopentanoate significantly altered the
pressor reflex (36 ± 3 to 25 ± 4 mmHg, P < 0.05, n = 5). Our combined data suggest that spinal
NMDA and AMPA receptors play a role in the abdominal ischemia
pressor reflex.
6-nitro-7-sulfamylbenzo(f)quinoxaline-2,3-dione; dl-2-amino-5-phosphonopentanoate;
-chloralose; decerebrate
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