Buchholz R A, Hubbard J W, Keeton T K, Nathan M A
Brain Res. 1986 Feb 19;365(2):360-4. doi: 10.1016/0006-8993(86)91650-1.
The cardiovascular and neuroendocrine responses to acute behavioral stress were evaluated in rats after disruption of the baroreflexes by electrolytic lesions of the nucleus tractus solitarii (NTS) or sinoaortic denervation (SAD). Rats with NTS lesions or SAD showed significantly greater increases in mean arterial pressure (MAP) and plasma norepinephrine (NE) concentrations than control rats during a single 30-min escape-avoidance test. In addition, the increases in MAP and plasma NE concentration of NTS lesion rats were significantly greater than those of SAD rats. However, NTS lesion rats showed no increase in plasma renin activity (PRA), as observed in the other groups. Thus, disruption of the baroreflexes by NTS lesions or SAD augments the arterial pressure and plasma NE responses to stress. Additionally, NTS lesions appeared to eliminate the neurons or fibers of passage participating in the sympathetically mediated increase in PRA.
在通过孤束核（NTS）电解损伤或去窦主动脉神经（SAD）破坏压力反射后，评估大鼠对急性行为应激的心血管和神经内分泌反应。在单次30分钟的逃避-回避试验中，患有NTS损伤或SAD的大鼠平均动脉压（MAP）和血浆去甲肾上腺素（NE）浓度的升高显著大于对照大鼠。此外，NTS损伤大鼠的MAP和血浆NE浓度升高显著大于SAD大鼠。然而，与其他组不同，NTS损伤大鼠的血浆肾素活性（PRA）没有增加。因此，NTS损伤或SAD破坏压力反射会增强动脉血压和血浆NE对应激的反应。此外，NTS损伤似乎消除了参与交感神经介导的PRA升高的神经元或传导纤维。
