Sanders Paul W
Nephrology Research and Training Center, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL 35294-0007, USA.
Hypertension. 2004 Feb;43(2):142-6. doi: 10.1161/01.HYP.0000114022.20424.22. Epub 2004 Jan 5.
It has been known for decades that increased dietary intake of salt (NaCl) shortens the life span of rats in a dose-dependent fashion. This review focuses specifically on the recently described biological effect and consequences of increased salt ingestion on the endothelium through a mechanism that is independent of blood pressure. Changes in salt intake are recognized by endothelial cells in the vascular tree and glomeruli through a physical process that promotes a series of signaling events involved in transcriptional regulation of genes that include transforming growth factor-beta1 (TGF-beta1) and the endothelial isoform of nitric oxide synthase (NOS3). A balance is struck between TGF-beta1 and NOS3 as salt intake varies and creates a negative feedback loop, because TGF-beta1 increased expression of NOS3 and NO inhibited production of TGF-beta1 in healthy rats. Changes in this feedback system have been observed in salt-sensitive hypertension and appear to impact end-organ damage, particularly the kidney. The data support an important benefit to reduction of salt intake in the setting of chronic kidney disease.
几十年来，人们已经知道，增加饮食中盐（氯化钠）的摄入量会以剂量依赖的方式缩短大鼠的寿命。本综述特别关注最近描述的通过一种独立于血压的机制增加盐摄入对内皮细胞的生物学效应和后果。血管树和肾小球中的内皮细胞通过一个促进一系列信号事件的物理过程识别盐摄入量的变化，这些信号事件参与包括转化生长因子-β1（TGF-β1）和内皮型一氧化氮合酶（NOS3）在内的基因的转录调控。随着盐摄入量的变化，TGF-β1和NOS3之间达成平衡并形成一个负反馈回路，因为在健康大鼠中，TGF-β1增加NOS3的表达，而一氧化氮（NO）抑制TGF-β1的产生。在盐敏感性高血压中已经观察到这种反馈系统的变化，并且似乎会影响靶器官损伤，尤其是肾脏。这些数据支持在慢性肾脏病患者中减少盐摄入量具有重要益处。
