Excessive activation of the sympathetic nervous system is one of the pathophysiological hallmarks of hypertension and heart failure. Within the central nervous system, the paraventricular nucleus (PVN) of the hypothalamus and the rostral ventrolateral medulla in the brain stem play critical roles in the regulation of sympathetic outflow to peripheral organs. Information from the peripheral circulation, including serum concentrations of sodium and angiotensin II, is conveyed to the PVN via adjacent structures with a weak blood–brain barrier. In addition, signals from baroreceptors, chemoreceptors and cardiopulmonary receptors as well as afferent input via the renal nerves are all integrated at the level of the PVN. The brain renin-angiotensin system and the balance between nitric oxide and reactive oxygen species in these brain areas also determine the final sympathetic outflow. Additionally, brain inflammatory responses have been shown to modulate these processes. Renal denervation interrupts both the afferent inputs from the kidney to the PVN and the efferent outputs from the PVN to the kidney, resulting in the suppression of sympathetic outflow and eliciting beneficial effects on both hypertension and heart failure.

交感神经系统的过度激活是高血压和心力衰竭的病理生理特征之一。在中枢神经系统中，下丘脑的室旁核 (PVN) 和脑干中的延髓头端腹外侧在调节交感神经流出到周围器官中起关键作用。来自外周循环的信息，包括钠和血管紧张素 II 的血清浓度，通过具有弱血脑屏障的相邻结构传递到 PVN。此外，来自压力感受器、化学感受器和心肺感受器的信号以及通过肾神经的传入输入都在 PVN 水平上整合。脑肾素-血管紧张素系统以及这些脑区一氧化氮和活性氧之间的平衡也决定了最终的交感神经流出。此外，大脑炎症反应已被证明可以调节这些过程。肾脏去神经支配中断从肾脏到 PVN 的传入输入和从 PVN 到肾脏的传出输出，导致交感神经外流的抑制，并对高血压和心力衰竭产生有益影响。