Neurotransmission of the cardiovascular reflexes in the nucleus tractus solitarii of awake rats.

Chemoreflex activation with potassium cyanide (i.v.) produces pressor and bradycardic responses in awake rats. Microinjection of AP-5, a selective NMDA receptor antagonist, into the nucleus tractus solitarii (NTS) produced a dose-dependent blockade of the bradycardic response; while microinjection of DNQX, a selective non-NMDA receptor antagonist, or kynurenic acid, a nonselective ionotropic receptor antagonist, produced only a partial reduction in the pressor response, indicating that the bradycardic component of the chemoreflex is mediated by NMDA receptors and that the sympathoexcitatory component may involve neurotransmitters other than excitatory amino acids. With respect to the baroreflex, we verified that the gain of baroreflex bradycardia in response to phenyleprine (Phe) infusion was significantly reduced in a dose-dependent manner by microinjection of AP-5 into the NTS, indicating that the parasympathetic component of the baroreflex is mediated mainly by NMDA receptors. However, in a series of experiments involving the electrical stimulation of the aortic depressor nerve (ADN) we observed that the maximal bradycardic response was almost blocked by the combination of microinjection of NMDA and non-NMDA receptor antagonists into the NTS, while the depressor response was only partially reduced. These data indicate that the bradycardic response produced by the activation of the baroreflex with Phe is mediated by mechanisms differing from those in response to the electrical stimulation of the ADN because phenylephrine also activates carotid and aortic baroreceptors, while unilateral electrical stimulation of the ADN involves only one specific set of baroreceptor afferents. These data also indicate that the sympatho inhibitory component of this response may involve neurotransmitters other than L-glutamate. We discuss the possibility that two different afferent systems of arterial baroreceptors are involved in the modulation of parasympathoexcitation and sympathoinhibition: one activated within the normal range of pulsatile arterial pressure (on a pulse-to-pulse basis) and the other acting under circumstances of challenge to the pulsatile arterial pressure above the normal range.