Angiotensin II receptors and peritoneal dialysis-induced peritoneal fibrosis

被引:9
|
作者
Morinelli, Thomas A. [1 ]
Luttrell, Louis M. [2 ,3 ]
Strungs, Erik G. [2 ]
Ullian, Michael E. [1 ,3 ]
机构
[1] Med Univ South Carolina, Dept Med, Div Nephrol, Charleston, SC 29425 USA
[2] Med Univ South Carolina, Div Endocrinol, Dept Med, Charleston, SC 29425 USA
[3] Ralph H Johnson Vet Affairs Med Ctr, Res Serv, Charleston, SC 29401 USA
基金
美国国家卫生研究院;
关键词
Angiotensin II; Arrestin; AT1R; Fibrosis; Peritoneal mesothelial cells; SMOOTH-MUSCLE-CELLS; PROTEIN-COUPLED RECEPTORS; GROWTH-FACTOR-BETA; NF-KAPPA-B; TYPE-1; RECEPTOR; AT(1) RECEPTOR; MESOTHELIAL CELLS; BLOOD-PRESSURE; HIGH GLUCOSE; NUCLEAR-LOCALIZATION;
D O I
10.1016/j.biocel.2016.04.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The vasoactive hormone angiotensin II initiates its major hemodynamic effects through interaction with AT1 receptors, a member of the class of G protein-coupled receptors. Acting through its AT1R, angiotensin II regulates blood pressure and renal salt and water balance. Recent evidence points to additional pathological influences of activation of AT1R, in particular inflammation, fibrosis and atherosclerosis. The transcription factor nuclear factor kappa B, a key mediator in inflammation and atherosclerosis, can be activated by angiotensin II through a mechanism that may involve arrestin-dependent AT1 receptor internalization. Peritoneal dialysis is a therapeutic modality for treating patients with end-stage kidney disease. The effectiveness of peritoneal dialysis at removing waste from the circulation is compromised over time as a consequence of peritoneal dialysis-induced peritoneal fibrosis. The non-physiological dialysis solution used in peritoneal dialysis, i.e. highly concentrated, hyperosmotic glucose, acidic pH as well as large volumes infused into the peritoneal cavity, contributes to the development of fibrosis. Numerous trials have been conducted altering certain components of the peritoneal dialysis fluid in hopes of preventing or delaying the fibrotic response with limited success. We hypothesize that structural activation of AT1R by hyperosmotic peritoneal dialysis fluid activates the internalization process and subsequent signaling through the transcription factor nuclear factor kappa B, resulting in the generation of pro-fibrotic/pro-inflammatory mediators producing peritoneal fibrosis. (C) 2016 Elsevier Ltd. All rights reserved.
引用
收藏
页码:240 / 250
页数:11
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