Amplification of Salt-Sensitive Hypertension and Kidney Damage by Immune Mechanisms

被引:14
作者
Mattson, David L. [1 ]
Dasinger, John Henry [1 ]
Abais-Battad, Justine M. [1 ]
机构
[1] Augusta Univ, Med Coll Georgia, Dept Physiol, Augusta, GA 30912 USA
基金
美国国家卫生研究院;
关键词
blood pressure; hypertension; immune cells; kidney; II-INDUCED HYPERTENSION; GENOME-WIDE ASSOCIATION; RENAL MEDULLARY H2O2; BLOOD-PRESSURE; T-CELL; OXIDATIVE STRESS; ATTENUATES HYPERTENSION; DENDRITIC CELLS; SODIUM SENSITIVITY; AFRICAN-AMERICANS;
D O I
10.1093/ajh/hpaa124
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Humans with salt-sensitive ( SS) hypertension demonstrate increased morbidity, increased mortality, and renal end-organ damage when compared with normotensive subjects or those with salt-resistant hypertension. Increasing evidence indicates that immune mechanisms play an important role in the full development of SS hypertension and associated renal damage. Recent experimental advances and studies in animal models have permitted a greater understanding of the mechanisms of activation and action of immunity in this disease process. Evidence favors a role of both innate and adaptive immune mechanisms that are triggered by initial, immune-independent alterations in blood pressure, sympathetic activity, or tissue damage. Activation of immunity, which can be enhanced by a high-salt intake or by alterations in other components of the diet, leads to the release of cytokines, free radicals, or other factors that amplify renal damage and hypertension and mediate malignant disease.
引用
收藏
页码:3 / 14
页数:12
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