In the halothane-anesthetized paralyzed rat, electrical or chemical stimulation of lateral hypothalamic sites dorsolateral to the fornix produced pressor effects, increases in lumbar sympathetic nerve discharge (SND), and excitation of the majority of bulbospinal sympathoexcitatory neurons of nucleus paragigantocellularis lateralis (PGCL sympathoexcitatory neurons). The relationship between SND and mean arterial pressure (MAP) was shifted upward by electrical hypothalamic stimulation, whereas the gain of the baroreflex was unchanged. A similar upward shift of the relationship between the discharge rate of PGCL sympathoexcitatory neurons and MAP was observed during stimulation. The excitatory effect of L-glutamate on PGCL sympathoexcitatory neurons was blocked by iontophoretic applications of kynurenic acid, whereas identical amounts of 8-OH kynurenic acid were ineffective. Bilateral pressure injections of kynurenic acid (but not of 8-OH kynurenic acid) into nucleus PGCL markedly reduced the pressor and sympathoexcitatory effects of hypothalamic stimulation without altering the on-going level of SND or its baroreflex inhibition. Applied by iontophoresis, kynurenic acid also attenuated the excitation of PGCL sympathoexcitatory neurons produced by hypothalamic stimulation. It is concluded that descending sympathoexcitatory pathways, originating in part in the lateral hypothalamus, relay in nucleus PGCL. This relay involves synapses that release an endogenous glutamate receptor agonist. These results suggest that synaptic integration between these glutamatergic inputs and gamma-aminobutyric acid baroreceptor inputs occurs in the immediate vicinity of PGCL bulbospinal sympathoexcitatory neurons or perhaps directly on their somadendritic surface.