Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA.
Nat Rev Nephrol. 2019 May;15(5):290-300. doi: 10.1038/s41581-019-0121-z.
Immune mechanisms have been recognized to have a role in the pathogenesis of hypertension, vascular disease and kidney damage in humans and animals for many decades. Contemporary advances in experimentation have permitted a deeper understanding of the mechanisms by which inflammation and immunity participate in cardiovascular disease, and multiple observations have demonstrated strong correlations between the discoveries made in animals and those made in patients with hypertension. Of note, striking phenotypic similarities have been observed in the infiltration of immune cells in the kidney and the development of end-organ damage in patients and animal models with sodium-sensitive hypertension. The available data suggest that an initial salt-induced increase in renal perfusion pressure, which is likely independent of immune mechanisms, induces the infiltration of immune cells into the kidney. The mechanisms mediating immune cell infiltration in the kidney are not well understood but likely involve tissue damage, the direct influence of salt to stimulate immune cell activation, sympathetic nerve stimulation or other factors. The infiltrating cells then release cytokines, free radicals and other factors that contribute to renal damage as well as increased retention of sodium and water and vascular resistance, which lead to the further development of hypertension.
几十年来，人们已经认识到免疫机制在人类和动物的高血压、血管疾病和肾脏损伤发病机制中起作用。实验的当代进展使人们能够更深入地了解炎症和免疫参与心血管疾病的机制，并且多项观察结果表明，在高血压患者和动物模型中，动物研究和临床研究之间存在很强的相关性。值得注意的是，在对钠敏感型高血压患者和动物模型的肾脏和终末器官损伤中，观察到免疫细胞浸润和发生的惊人表型相似性。现有数据表明，最初的盐诱导的肾灌注压增加可能独立于免疫机制，诱导免疫细胞浸润肾脏。介导肾脏免疫细胞浸润的机制尚不清楚，但可能涉及组织损伤、盐直接刺激免疫细胞激活、交感神经刺激或其他因素。然后，浸润的细胞释放细胞因子、自由基和其他因子，导致肾脏损伤以及钠和水潴留增加和血管阻力增加，从而进一步发展为高血压。
