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AJP - Regulatory, Integrative and Comparative Physiology, Vol 273, Issue 2 487-R494, Copyright © 1997 by American Physiological Society
ARTICLES |
S. Ito and A. F. Sved
Department of Neuroscience, University of Pittsburgh, Pennsylvania 15260, USA.
Sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) play a key role in the tonic maintenance of resting arterial pressure. Removal of tonically active inhibitory inputs to the RVLM provided by the caudal ventrolateral medulla (CVLM) elicits a large increase in arterial pressure. The present study addresses the hypothesis that excitatory amino acids (EAA) provide the excitation of the RVLM responsible for the increase in arterial pressure that occurs after withdrawal of CVLM-mediated inhibition of the RVLM. In rats anesthetized with either alpha-chloralose or urethan, inhibition of the CVLM by local injection of muscimol markedly elevated arterial pressure. Subsequent injection of the EAA receptor antagonist kynurenic acid into the RVLM caused arterial pressure to fall to levels comparable to those that occur-with total autonomic blockade. In contrast, injection of kynurenic acid into the RVLM of control rats had little effect on arterial pressure. These results indicate that the large increase in arterial pressure produced by inhibition of the CVLM is mediated by EAA excitation of RVLM neurons. Furthermore, these data suggest that EAA play a prominent role in the tonic excitation of RVLM neurons, but, in intact rats, inhibition of EAA in the RVLM elicits no change in arterial pressure because of removal of inhibitory as well as excitatory drives of the RVLM.
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