Salt, Hypertension, and Immunity

被引:96
作者
Rucker, A. Justin [1 ,2 ]
Rudemiller, Nathan P. [1 ,2 ]
Crowley, Steven D. [1 ,2 ]
机构
[1] Duke Univ, Sch Med, Dept Med, Div Nephrol, Durham, NC 27710 USA
[2] Durham Vet Affairs Med Ctr, Durham, NC 27705 USA
来源
ANNUAL REVIEW OF PHYSIOLOGY, VOL 80 | 2018年 / 80卷
基金
美国国家卫生研究院;
关键词
sodium; macrophage; monocyte; T cells; dendritic cells; cytokines; TUMOR-NECROSIS-FACTOR; II-INDUCED HYPERTENSION; COLONY-STIMULATING FACTOR; BLOOD-PRESSURE REGULATION; RENIN-ANGIOTENSIN SYSTEM; DENDRITIC CELL SUBSETS; HUMAN T-CELLS; OXIDATIVE STRESS; RENAL INJURY; SENSITIVE HYPERTENSION;
D O I
10.1146/annurev-physiol-021317-121134
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The link between inappropriate salt retention in the kidney and hypertension is well recognized. However, growing evidence suggests that the immune system can play surprising roles in sodium homeostasis, such that the study of inflammatory cells and their secreted effectors has provided important insights into salt sensitivity. As part of the innate immune system, myeloid cells have diverse roles in blood pressure regulation, ranging from prohypertensive actions in the kidney, vasculature, and brain, to effects in the skin that attenuate blood pressure elevation. In parallel, T lymphocyte subsets, as key constituents of the adaptive immune compartment, have variable effects on renal sodium handling and the hypertensive response, accruing from the functions of the cytokines that they produce. Conversely, salt can directly modulate the phenotypes of myeloid and T cells, illustrating bidirectional regulatory mechanisms through which sodium and the immune system coordinately impact blood pressure. This review details the complex interplay between myeloid cells, T cells, and salt in the pathogenesis of essential hypertension.
引用
收藏
页码:283 / 307
页数:25
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