Istituto Auxologico Italiano, IRCCS, Department of Cardiovascular, Neural and Metabolic Sciences, San Luca Hospital, Milan, Italy.
Departamento de Química Biológica, IQUIFIB-CONICET, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.
Nat Rev Cardiol. 2019 Aug;16(8):476-490. doi: 10.1038/s41569-019-0178-1.
Hypertension is an important risk factor for cardiovascular morbidity and mortality and for events such as myocardial infarction, stroke, heart failure and chronic kidney disease and is a major determinant of disability-adjusted life-years. Despite the importance of hypertension, the pathogenesis of essential hypertension, which involves the complex interaction of several mechanisms, is still poorly understood. Evidence suggests that interplay between bone marrow, microglia and immune mediators underlies the development of arterial hypertension, in particular through mechanisms involving cytokines and peptides, such as neuropeptide Y, substance P, angiotensin II and angiotensin-(1-7). Chronic psychological stress also seems to have a role in increasing the risk of hypertension, probably through the activation of neuroimmune pathways. In this Review, we summarize the available data on the possible role of neuroimmune crosstalk in the origin and maintenance of arterial hypertension and discuss the implications of this crosstalk for recovery and rehabilitation after cardiac and cerebral injuries.
高血压是心血管发病率和死亡率的重要危险因素,也是心肌梗死、中风、心力衰竭和慢性肾病等事件的重要决定因素,并且是导致伤残调整生命年的主要因素。尽管高血压很重要,但涉及多种机制复杂相互作用的原发性高血压的发病机制仍知之甚少。有证据表明,骨髓、小胶质细胞和免疫介质之间的相互作用是动脉高血压发展的基础,特别是通过涉及细胞因子和肽的机制,如神经肽 Y、P 物质、血管紧张素 II 和血管紧张素-(1-7)。慢性心理应激似乎也在增加高血压的风险方面发挥作用,可能是通过激活神经免疫途径。在这篇综述中,我们总结了有关神经免疫串扰在动脉高血压起源和维持中可能作用的现有数据,并讨论了这种串扰对心脏和大脑损伤后恢复和康复的影响。