血管迷走性晕厥（vasovagal syncope, VVS）是临床上最常见的晕厥类型，主要由自主神经系统对外界刺激反应过度引起，导致血管扩张和心动过缓，从而引起全脑灌注降低。目前VVS的病理生理机制仍存在较多未知，神经体液调节机制在其中发挥重要作用。交感神经系统（sympathetic nervous system, SNS）通过调节心率、血压和血管张力，在VVS的发生中起重要作用，尤其是在血压调节、体位变化和应激反应等方面。肾素-血管紧张素-醛固酮系统（renin-angiotensin-aldosterone system, RAAS）通过调节血管收缩和钠水潴留，维持血容量和血压的稳定。血管内皮细胞分泌的一氧化氮（nitric oxide, NO）、硫化氢（hydrogen sulfide, H₂S）作为血管舒张因子，以及内皮素（Endothelin, ET）作为血管收缩因子，均参与调节血管张力。神经递质如5-羟色胺（5-Hydroxytryptamine, 5-HT）和甘丙肽也在VVS的发生中起到重要作用。SNS和RAAS参与了VVS的发生过程，在血流动力学尚处于稳定状态时，血浆肾上腺素（epinephrine，Epi）和去甲肾上腺素（norepinephrine，NE）浓度升高，Epi增量远高于NE，致使Epi/NE值增加，显著的β肾上腺素能效应导致外周血管扩张，静脉血流蓄积，出现进行性的血压下降，成为导致晕厥发生最重要的病理生理机制。而在低血压发生时，机体代偿性分泌大量抗利尿激素（arginine Vasopressin，AVP），显著AVP浓度升高反而进一步导致血管舒张，加剧血压下降，致使晕厥发生。未来更精准的VVS药物开发将成为重点，利用现代药理学和分子生物学技术，针对特定神经体液机制，开发出更高效且副作用更少的药物；其次寻找和验证新的生物标志物将推动早期诊断和治疗效果监测的进步。

Vasovagal syncope (VVS) is the most common type of syncope in clinical practice, primarily caused by the excessive response of the autonomic nervous system to external stimuli, leading to vasodilation and bradycardia, and consequently reduced whole brain perfusion. At present, the pathophysiological mechanism of VVS remains largely unknown, with neurohumoral regulation playing a significant role in it. Sympathetic Nervous System (SNS) plays a crucial role in the occurrence of VVS by regulating heart rate, blood pressure and vascular tone, especially in blood pressure regulation, postural changes, and stress response. The Renin-Angiotensin-Aldosterone System (RAAS) maintains blood volume and blood pressure stability by regulating vasoconstriction and sodium and water retention. Nitric oxide (NO) and hydrogen sulfide (H₂S) secreted by vascular endothelial cells as vasodilator factors, and Endothelin (ET) as vasoconstrictor factors, are involved in regulating vascular tone. Neurotransmitters such as 5-hydroxytryptamine (5-HT) and galanin also play a key role in the occurrence of VVS. SNS and RAAS are involved in the occurrence of VVS. When the hemodynamics is still in a stable state, the plasma Epi and NE concentrations increase, and the Epi increment is much higher than NE, resulting in an increase in Epi/NE value. The significant β-adrenergic effect leads to peripheral vasodilation, venous blood flow accumulation, and progressive blood pressure decline, which is the most important pathophysiological mechanism leading to syncope. When hypotension occurs, the body compensatively secretes a large amount of AVP, and the significant increase of AVP concentration further leads to vasodilation, aggravates the decrease of blood pressure, and causes syncope. In the future, more accurate VVS drug development will become the focus. Using modern pharmacology and molecular biology techniques, drugs targeting specific neurohumoral mechanisms will be developed to achieve higher efficacy with fewer side effects. Additionally, the identification and validation of new biomarkers will drive advancements in early diagnosis and monitoring of treatment outcomes.