Itani Hana A, Harrison David G
Division of Clinical Pharmacology, Department of Medicine, School of Medicine, Vanderbilt University, Nashville, Tennessee
Division of Clinical Pharmacology, Department of Medicine, School of Medicine, Vanderbilt University, Nashville, Tennessee.
Am J Physiol Renal Physiol. 2015 Jun 1;308(11):F1197-9. doi: 10.1152/ajprenal.00633.2014. Epub 2015 Apr 1.
In recent years, it has become clear that the immune system contributes to the genesis of hypertension. Hypertensive stimuli, such as angiotensin II, DOCA-salt, and norepinephrine, cause T cells and monocytes/macrophages to accumulate in the kidney and vasculature. These cells release inflammatory cytokines, such as IL-6, interferon-γ, and IL-17, that promote renal and vascular dysfunction. These cytokines also promote angiotensinogen production in the proximal tubule and Na(+) retention in the distal nephron and contribute to renal fibrosis and glomerular damage. For several years, we have observed accumulation of memory T cells in the kidney and vasculature. Given the propensity for memory cells to produce cytokines such as interferon-γ and IL-17, interventions to prevent the formation or renal accumulation of specific memory T cell subsets could prevent end-organ damage and blood pressure elevation in response to hypertensive stimuli.
近年来，免疫系统在高血压发病机制中的作用已逐渐明晰。诸如血管紧张素II、去氧皮质酮盐和去甲肾上腺素等高血压刺激因素，会致使T细胞以及单核细胞/巨噬细胞在肾脏和血管系统中积聚。这些细胞会释放白细胞介素-6、干扰素-γ和白细胞介素-17等炎性细胞因子，进而引发肾脏和血管功能障碍。这些细胞因子还会促进近端肾小管中血管紧张素原的生成以及远端肾单位中钠的潴留，并促使肾纤维化和肾小球损伤。多年来，我们观察到记忆性T细胞在肾脏和血管系统中积聚。鉴于记忆细胞具有产生干扰素-γ和白细胞介素-17等细胞因子的倾向，采取干预措施以阻止特定记忆T细胞亚群的形成或在肾脏中的积聚，或许能够预防终末器官损伤以及因高血压刺激而导致的血压升高。
