Barnes K L, Ferrario C M
Hypertension. 1984 Jul-Aug;6(4):482-8. doi: 10.1161/01.hyp.6.4.482.
Electrical stimulation of the dog's area postrema (AP) induces a response that mimics the pressor response produced by intravertebral infusion of low-dose angiotensin II, which causes an increase in mean arterial pressure associated with transient tachycardia and increased peripheral resistance. The present study investigated in morphine-chloralose anesthetized dogs whether: 1) the characteristics of the AP pressor response are influenced by the presence of carotid sinus afferents; 2) structures rostral to the medulla influence the AP pressor response; and 3) the pressor pathway is initiated by neurons within the AP. Since bilateral cervical sinovagal denervation, which potentiated the phenylephrine pressor response, did not affect the pressor response to AP stimulation, the data provide evidence for an inhibitory influence exerted upon the central baroreflex mechanism by the AP pressor mechanism. The unaltered AP pressor response after midcollicular transection suggests that the efferent pathway is contained within the brain stem caudal to the pons. Finally, the elimination of the pressor response following kainic acid microinjection into the AP provides evidence that the AP pressor mechanism is initiated by neurons within the AP, rather than by fibers of passage from other pressor centers. These results suggest that the AP produces its facilitation of central sympathetic vasomotor outflow via a pathway contained within the medulla.
对犬最后区（AP）进行电刺激会引发一种反应，该反应类似于经椎管内注入低剂量血管紧张素II所产生的升压反应，后者会导致平均动脉压升高，并伴有短暂性心动过速和外周阻力增加。本研究在吗啡 - 氯醛糖麻醉的犬中探究了：1）颈动脉窦传入神经的存在是否会影响AP升压反应的特征；2）延髓上方的结构是否会影响AP升压反应；3）升压途径是否由AP内的神经元启动。由于双侧颈迷走神经切断术增强了去氧肾上腺素的升压反应，但并未影响对AP刺激的升压反应，这些数据为AP升压机制对中枢压力反射机制施加抑制性影响提供了证据。中脑横断术后AP升压反应未改变，这表明传出途径包含在脑桥尾侧的脑干内。最后，向AP内微量注射 kainic 酸后升压反应消失，这证明AP升压机制是由AP内的神经元启动的，而非来自其他升压中枢的传入纤维。这些结果表明，AP通过延髓内的一条途径促进中枢交感血管运动输出。
