Prat Hernán, Araos Patricio, Michea Luis
Departamento Cardiovascular, Facultad de Medicina, Universidad de Chile, Santiago, Chile.
Laboratorio de Fisiopatología Renal, Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile.
Rev Med Chil. 2021 Feb;149(2):255-262. doi: 10.4067/s0034-98872021000200255.
Even though the mechanisms that mediate essential hypertension (HT) are not fully understood, an immunological-inflammatory mechanism could be the common pathway for diverse pathophysiological mechanisms. We analyze in a simplified way the participation of the immune system in HT. T lymphocytes (TL) and antigen presenting cells (APCs) are components of the immune system capable of generating proinflammatory cytokines. They cause endothelial damage, vasoconstriction, and decreased urinary sodium excretion. CD4+ and CD8+ TL are effector cells, causally implicated in the development of HT, whereas type γδ TL play their pathogenic role in HT enhancing endothelial dysfunction. Additionally, a immunomodulation decrease by regulatory TL, worsens endothelial dysfunction and reduces vasodilation in experimental HT. Results of recent studies indicate that lymphocyte activation would be mediated by antigens captured by antigen APCs for subsequent presentation to "naive" TL. On the other hand, proinflammatory states such as obesity, the change of the intestinal microbiota and the increase in salt intake favors TL and APC activation, contributing to HT development.
尽管介导原发性高血压（HT）的机制尚未完全明确，但免疫 - 炎症机制可能是多种病理生理机制的共同途径。我们以简化的方式分析免疫系统在高血压中的作用。T淋巴细胞（TL）和抗原呈递细胞（APC）是免疫系统的组成部分，能够产生促炎细胞因子。它们会导致内皮损伤、血管收缩以及尿钠排泄减少。CD4 +和CD8 + TL是效应细胞，与高血压的发生有因果关系，而γδ型TL在高血压中通过增强内皮功能障碍发挥其致病作用。此外，调节性TL导致的免疫调节功能下降会使实验性高血压中的内皮功能障碍恶化并减少血管舒张。近期研究结果表明，淋巴细胞激活可能由抗原呈递细胞捕获抗原后呈递给“未致敏”TL介导。另一方面，肥胖、肠道微生物群变化和盐摄入量增加等促炎状态有利于TL和APC的激活，从而促进高血压的发展。
