AUTONOMIC PROCESSING OF THE CARDIOVASCULAR REFLEXES IN THE NUCLEUS-TRACTUS-SOLITARII

Citation
Bh. Machado et al., AUTONOMIC PROCESSING OF THE CARDIOVASCULAR REFLEXES IN THE NUCLEUS-TRACTUS-SOLITARII, Brazilian journal of medical and biological research, 30(4), 1997, pp. 533-543
Citations number
52
Categorie Soggetti
Medicine, Research & Experimental
ISSN journal
0100879X
Volume
30
Issue
4
Year of publication
1997
Pages
533 - 543
Database
ISI
SICI code
0100-879X(1997)30:4<533:APOTCR>2.0.ZU;2-1
Abstract
The nucleus tractus solitarii (NTS) receives afferent projections from the arterial baroreceptors, carotid chemoreceptors and cardiopulmonar y receptors and as a function of this information produces autonomic a djustments in order to maintain arterial blood pressure within a narro w range of variation. The activation of each of these cardiovascular a fferents produces a specific autonomic response by the excitation of n euronal projections from the NTS to the ventrolateral areas of the med ulla (nucleus ambiguus, caudal and rostral ventrolateral medulla). The neurotransmitters at the NTS level as well as the excitatory amino ac id (EAA) receptors involved in the processing of the autonomic respons es in the NTS, although extensively studied, remain to be completely e lucidated, In the present review we discuss the role of the EAA L-glut amate and its different receptor subtypes in the processing of the car diovascular reflexes in the NTS. The data presented in this review rel ated to the neurotransmission in the NTS are based on experimental evi dence obtained in our laboratory in unanesthetized rats. The two major conclusions of the present review are that a) the excitation of the c ardiovagal component by cardiovascular reflex activation (chemo- and B ezold-Jarisch reflexes) or by L-glutamate microinjection into the NTS is mediated by N-methyl-D-aspartate (NMDA) receptors, and b) the sympa tho-excitatory component of the chemoreflex and the presser response t o L-glutamate microinjected into the NTS are not affected by an NMDA r eceptor antagonist, suggesting that the sympatho-excitatory component of these responses is mediated by non-NMDA receptors.