Aging of the cardiovascular regulatory function manifests as an imbalance between the sympathetic and parasympathetic (vagal) components of the autonomic nervous system (ANS). The most characteristic change is sympathetic overdrive, which is manifested by an increase in the muscle sympathetic nerve activity (MSNA) burst frequency with age. Age-related changes that occur in vagal nerve activity is less clear. The resting tonic parasympathetic activity can be estimated noninvasively by measuring the increase in heart rate occurring in response to muscarinic cholinergic receptor blockade; animal study models have shown this to diminish with age. Humoral, cellular, and neural mechanisms work together to prevent non-resolving inflammation. This review focuses on the mechanisms underlying age-related alternations in the ANS and how an imbalance in the ANS, evaluated by MSNA and heart rate variability (HRV), potentially facilitates inflammation when the homeostatic mechanisms between reflex neural circuits and the immune system are compromised, particularly the dysfunction of the cholinergic anti-inflammatory reflex. Physiologically, the efferent arm of this reflex acts via the \(\alpha\) 7 nicotinic acetylcholine receptors expressed in macrophages, monocytes, dendritic cells, T cells, and endothelial cells to curb the release of inflammatory cytokines, in which inhibition of NF‑κB nuclear translocation and activation of a JAK/STAT-mediated signaling cascade in macrophages and other immune cells are implicated. This reflex is likely to become less adequate with advanced age. Consequently, a pro-inflammatory state induced by reduced vagus output with age is associated with endothelial dysfunction and may significantly contribute to the development and propagation of atherosclerosis, heart failure, and hypertension. The aim of this review is to summarize the relationship between ANS dysfunction, inflammation, and endothelial dysfunction in the context of aging. Meanwhile, this review also attempts to describe the role of HRV measures as a predictor of the level of inflammation and endothelial dysfunction in the aged population and explore the possible therapeutical effects of vagus nerve stimulation.

心血管调节功能的老化表现为自主神经系统（ANS）的交感神经和副交感神经（迷走神经）成分之间的不平衡。最典型的变化是交感神经过度兴奋，表现为肌肉交感神经活动（MSNA）爆发频率随着年龄的增长而增加。迷走神经活动与年龄相关的变化尚不清楚。通过测量响应毒蕈碱胆碱能受体阻断而发生的心率增加，可以无创地估计静息强直副交感神经活动；动物研究模型表明这种现象会随着年龄的增长而减弱。体液、细胞和神经机制共同作用，防止无法消退的炎症。本综述重点关注 ANS 中与年龄相关的变化的潜在机制，以及当反射神经回路和免疫系统之间的稳态机制受到损害时，通过 MSNA 和心率变异性 (HRV) 评估的 ANS 失衡如何可能促进炎症特别是胆碱能抗炎反射功能障碍。生理学上，这种反射的传出臂通过巨噬细胞、单核细胞、树突状细胞、T细胞和内皮细胞中表达的\(\alpha\) 7烟碱乙酰胆碱受体发挥作用，抑制炎症细胞因子的释放，其中抑制NF-巨噬细胞和其他免疫细胞中的 κB 核转位和 JAK/STAT 介导的信号级联的激活都与此有关。随着年龄的增长，这种反射可能会变得不那么充分。因此，随着年龄的增长，迷走神经输出减少引起的促炎症状态与内皮功能障碍相关，并且可能显着促进动脉粥样硬化、心力衰竭和高血压的发展和传播。本综述的目的是总结衰老背景下 ANS 功能障碍、炎症和内皮功能障碍之间的关系。同时，本综述还试图描述HRV测量作为老年人群炎症和内皮功能障碍水平的预测因子的作用，并探讨迷走神经刺激的可能治疗效果。