Chianca D A, Machado B H
Department of Biological Sciences, Federal University of Ouro Preto, MG, Brazil.
Brain Res. 1996 Apr 29;718(1-2):185-8. doi: 10.1016/0006-8993(96)00010-8.
The purpose of the present study was to evaluate whether or not cardiovagal excitatory and sympatho-inhibitory pathways of the Bezold-Jarisch reflex at the NTS level were mediated by NMDA receptors. The Bezold-Jarisch reflex was activated by intravenous (i.v.) injection of serotonin in conscious rats before and after microinjection of phosphonovaleric acid (AP-5) a selective NMDA antagonist, into the NTS. The Bezold-Jarisch reflex was also activated before and after methyl-atropine (i.v.) in order to evaluate if the changes in mean arterial pressure were dependent on the bradycardic response. The data showed that AP-5 into the NTS produced a dose-dependent reduction in both bradycardic and hypotensive responses to activation of the Bezold-Jarisch reflex. Methyl-atropine also blocked the bradycardic and hypotensive responses to Bezold-Jarisch reflex activation. The data show that in conscious rats the cardiovagal component of the Bezold-Jarisch reflex plays a major role in the cardiovascular changes produced by the activation of this reflex and suggest that the neurotransmission of the cardiovagal component of the Bezold-Jarisch reflex is mediated by NMDA receptors.
本研究的目的是评估孤束核水平的贝佐尔德-雅里什反射的心迷走兴奋和交感抑制通路是否由NMDA受体介导。在向孤束核微量注射选择性NMDA拮抗剂膦酰戊酸(AP-5)之前和之后,通过静脉注射5-羟色胺激活清醒大鼠的贝佐尔德-雅里什反射。为了评估平均动脉压的变化是否依赖于心动过缓反应,在静脉注射甲基阿托品之前和之后也激活了贝佐尔德-雅里什反射。数据显示,向孤束核注射AP-5可使对贝佐尔德-雅里什反射激活的心动过缓和低血压反应产生剂量依赖性降低。甲基阿托品也阻断了对贝佐尔德-雅里什反射激活的心动过缓和低血压反应。数据表明,在清醒大鼠中,贝佐尔德-雅里什反射的心迷走成分在该反射激活所产生的心血管变化中起主要作用,并提示贝佐尔德-雅里什反射的心迷走成分的神经传递由NMDA受体介导。