The nucleus of the tractus solitarius (NTS) is the central termination site of peripheral baroreceptor afferents. It has been suggested that the excitatory amino acid (EAA) L-glutamate may be a neurotransmitter which mediates transmission of baroreceptor information in the rat NTS. The present studies examined this hypothesis by pharmacological blockade of EAA receptors in the NTS. Bilateral microinjections into the NTS of the EAA receptor antagonist kynurenic acid (KYN) virtually abolished baroreflexes elicited by electrical stimulation of the aortic nerve. In addition, hypotension and bradycardia evoked by injections into the NTS of the selective EAA receptor agonists N-methyl-D-aspartate, kainate and the quisqualate-selective agonist, alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid were reduced by 75% or more after KYN. Paradoxically, KYN did not reduce cardiovascular responses produced by injections into the NTS of L-glutamate. These results demonstrate that 1) blockade of EAA receptors in the NTS is sufficient to abolish synaptically mediated aortic baroreflexes; 2) cardiovascular responses evoked by L-glutamate are not reduced after documented blockade of N-methyl-D-aspartate, kainate and quisqualate receptors in the NTS by KYN; and 3) under the conditions of these experiments, the pharmacological actions of exogenously administered L-glutamate are not identical to those of the neurotransmitter which is released at NTS synapses by aortic nerve stimulation. These observations suggest that an EAA or EAA analog other than L-glutamate may be the neurotransmitter of baroreceptor information in the NTS.

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