MECHANISMS OF PRESSER AND BRADYCARDIAC RESPONSES TO L-GLUTAMATE MICROINJECTED INTO THE NTS OF CONSCIOUS RATS

Microinjection of increasing doses of L-glutamate (L-Glu, 0.03-5.0 nmo 1/100 nl) into the nucleus tractus solitarii (NTS) produced a dose-rel ated presser and bradycardic response. Prazosin virtually abolished th e presser response but produced no changes in the bradycardic response to L-Glu, indicating that bradycardia is not reflex in origin. The br adycardic response was blocked by atropine. In three different groups of rats, excitatory amino acid receptors in the NTS were blocked by in creasing doses of kynurenic acid (0.5, 2.0, and 10.0 nmo1/100 nl) and the presser and bradycardic responses to L-Glu (1 nmo1/100 nl) were re duced in a dose-related pattern. Reflex bradycardia induced by an incr ease in pressure caused by phenylephrine (iv) was also blocked by kynu renic acid. These data show that microinjection of L-Glu into the NTS of conscious rats produced presser and bradycardic responses, which ar e due to the activation of two independent autonomic pathways. The dat a also indicate that the activation of both pathways is mediated by ex citatory amino acid receptors. Considering that reflex bradycardia was also blocked by kynurenic acid, we suggest that L-Glu and excitatory amino acid receptors are part of the parasympathetic limb of the baror eceptor reflex. The presser response to L-Glu is also mediated by exci tatory amino acid receptors, but its physiological meaning is still un clear.