Chemical stimulation of the kidney increases sympathetic activity and blood pressure in rats. The hypothalamic paraventricular nucleus (PVN) is important in mediating the excitatory renal reflex (ERR). In this study, we examined the role of molecular signaling in the PVN in mediating the capsaicin-induced ERR and sympathetic activation. Bilateral PVN microinjections were performed in rats under anesthesia. The ERR was elicited by infusion of capsaicin into the cortico-medullary border of the right kidney. The reflex was evaluated as the capsaicin-induced changes in left renal sympathetic nerve activity and mean arterial pressure. Blockade of angiotensin type 1 receptors with losartan or inhibition of angiotensin-converting enzyme with captopril in the PVN abolished the capsaicin-induced ERR. Renal infusion of capsaicin significantly increased NAD(P)H oxidase activity and superoxide anion production in the PVN, which were prevented by ipsilateral renal denervation or microinjection of losartan into the PVN. Furthermore, either scavenging of superoxide anions or inhibition of NAD(P)H oxidase in the PVN abolished the capsaicin-induced ERR. We conclude that the ERR induced by renal infusion of capsaicin is mediated by angiotensin type 1 receptor-related NAD(P)H oxidase activation and superoxide anion production within the PVN.

中文翻译：

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下丘脑室旁核中的血管紧张素1型受体和超氧阴离子的产生有助于辣椒素诱导的兴奋性肾反射和交感神经激活。

肾脏的化学刺激会增加大鼠的交感神经活动和血压。下丘脑室旁核（PVN）在介导兴奋性肾反射（ERR）中很重要。在这项研究中，我们检查了分子信号在PVN中介导辣椒素诱导的ERR和交感神经激活的作用。在麻醉下在大鼠中进行双侧PVN显微注射。通过向右肾的皮质-髓质边界注入辣椒素引发ERR。辣椒素引起的左肾交感神经活性和平均动脉压的变化被评估为反射。用氯沙坦阻断1型血管紧张素受体或用卡托普利抑制PVN抑制血管紧张素转化酶，消除了辣椒素诱导的ERR。肾脏输注辣椒素可显着增加PVN中的NAD（P）H氧化酶活性和超氧阴离子产生，这可通过同侧肾脏去神经或将氯沙坦微注射到PVN中来预防。此外，清除PVN中的超氧阴离子或抑制NAD（P）H氧化酶均消除了辣椒素诱导的ERR。我们得出的结论是，辣椒素的肾输注引起的ERR是由1型血管紧张素受体相关的NAD（P）H氧化酶激活和PVN内的超氧阴离子产生的。