Orthostatic hypotension is one of the most common symptoms observed in Parkinson's disease (PD), a neurodegenerative disease caused by death of dopaminergic neurons in the substantia nigra pars compacta (SNc), and it is associated with denervation of the heart and impairment of the baroreflex. Here, we aimed to investigate if the impaired baroreflex was associated with lower activation of cardiovascular brainstem areas in a 6-hydroxydopamine (6-OHDA) animal model of PD. The PD model was generated with male Wistar rats by injection of 6-OHDA or vehicle into the striatum. After 20 or 60 days, the femoral vein and artery were cannulated to assess cardiovascular parameters during injection of sodium nitroprusside (SNP) or phenylephrine (Phe). Brainstem slices were submitted to immunohistochemistry and immunofluorescence. After 6-OHDA injection, 75% of the dopaminergic neurons in the SNc were absent, confirming establishment of the PD model. Intravenous (iv) injection of SNP generated reduced hypotension and tachycardia response, and the noncatecholaminergic (nonC1) neurons of the rostral ventrolateral medulla (RVLM) were less activated. Additionally, iv injection of Phe increased blood pressure and bradycardia to the same extent and activated equivalent numbers of neurons in the nucleus of the solitary tract and the caudal ventrolateral medulla as well as cholinergic neurons of the dorsal motor nucleus of the vagus and the nucleus ambiguus between control and PD animals. In summary, these data showed that in the PD model, impairment of cardiovascular autonomic control was observed only during deactivation of the baroreflex, which could be related to reduced activation of non-C1 neurons within the RVLM.

中文翻译：

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帕金森病动物模型中压力反射减弱与非 C1 神经元激活受损相一致

直立性低血压是帕金森病 (PD) 中最常见的症状之一，帕金森病是一种由黑质致密部 (SNc) 中多巴胺能神经元死亡引起的神经退行性疾病，它与心脏去神经支配和压力反射受损有关. 在这里，我们旨在研究压力反射受损是否与 PD 的 6-羟基多巴胺 (6-OHDA) 动物模型中心血管脑干区域的低激活有关。通过将 6-OHDA 或载体注射到纹状体中，用雄性 Wistar 大鼠产生 PD 模型。20 或 60 天后，在注射硝普钠 (SNP) 或去氧肾上腺素 (Phe) 期间，将股静脉和动脉插管以评估心血管参数。脑干切片进行免疫组织化学和免疫荧光。6-OHDA 注射后，SNc 中 75% 的多巴胺能神经元不存在，证实了 PD 模型的建立。静脉 (iv) 注射 SNP 降低了低血压和心动过速反应，并且延髓腹外侧 (RVLM) 的非儿茶酚胺能 (nonC1) 神经元被较少激活。此外，静脉注射 Phe 使血压和心动过缓增加到相同的程度，并激活了孤立束核和尾部腹外侧髓质中等量的神经元以及迷走神经背运动核和模糊核的胆碱能神经元控制和 PD 动物之间。总之，这些数据表明，在 PD 模型中，仅在压力反射失活期间观察到心血管自主神经控制受损，