Abstract：
The sensitization and hypertonicity of visceral afferents are highly relevant to the development and progression of cardiovascular and respiratory disease states. In this review, we described the evidence that the inflammatory process regulates visceral afferent sensitivity and tonicity, affecting the control of the cardiovascular and respiratory system. Some inflammatory mediators like nitric oxide, angiotensin II, endothelin-1, and arginine vasopressin may inhibit baroreceptor afferents and contribute to the baroreflex impairment observed in cardiovascular diseases. Cytokines may act directly on peripheral afferent terminals that transmit information to the central nervous system (CNS). TLR-4 receptors, which recognize lipopolysaccharide, were identified in the nodose and petrosal ganglion and have been implicated in disrupting the blood-brain barrier, which can potentiate the inflammatory process. For example, cytokines may cross the blood-brain barrier to access the CNS. Additionally, pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α and some of their receptors have been identified in the nodose ganglion and carotid body. These pro-inflammatory cytokines also sensitize the dorsal root ganglion or are released in the nucleus of the solitary tract. In cardiovascular disease, pro-inflammatory mediators increase in the brain, heart, vessels, and plasma and may act locally or systemically to activate/sensitize afferent nervous terminals. Recent evidence demonstrated that the carotid body chemoreceptor cells might sense systemic pro-inflammatory molecules, supporting the novel proposal that the carotid body is part of the afferent pathway in the central anti-inflammatory reflexes. The exact mechanisms of how pro-inflammatory mediators affects visceral afferent signals and contribute to the pathophysiology of cardiovascular diseases awaits future research.
摘要：
内脏传入的致敏和高张性与心血管和呼吸道疾病状态的发展和进展高度相关。在这次审查中,我们描述了炎症过程调节内脏传入敏感性和张力的证据，影响心血管和呼吸系统的控制。一些炎症介质，如一氧化氮，血管紧张素II，内皮素-1和精氨酸加压素可以抑制压力感受器传入，并有助于心血管疾病中观察到的压力反射损害。细胞因子可直接作用于向中枢神经系统(CNS)传递信息的外周传入终端。TLR-4受体,识别脂多糖，在结状神经节和岩状神经节中发现，并与破坏血脑屏障有关，可以加强炎症过程。例如,细胞因子可能穿过血脑屏障进入中枢神经系统。此外,促炎细胞因子，如IL-1β，IL-6，TNF-α及其一些受体已在结节性神经节和颈动脉体中得到鉴定。这些促炎细胞因子还使背根神经节敏感或在孤束核中释放。在心血管疾病中，大脑中的促炎介质增加，心,船只,和血浆，并可能在局部或全身起作用以激活/敏感传入神经末梢。最近的证据表明，颈动脉体化学感受器细胞可能会感觉到全身的促炎分子，支持颈动脉体是中枢抗炎反射传入途径的一部分的新提议。促炎介质如何影响内脏传入信号并有助于心血管疾病病理生理学的确切机制有待进一步研究。
