계명대학교 의학도서관 Repository

Angiotensin II Removes Kidney Resistance Conferred by Ischemic Preconditioning

Metadata Downloads
Author(s)
Hee-Seong JangJee In KimJinu KimJeen-Woo ParkKwon Moo Park
Publication Year
2014
Abstract
Ischemic preconditioning (IPC) by ischemia/reperfusion (I/R) renders resistance to the kidney. Strong IPC triggers kidney fibrosis, which is involved in angiotensin II (AngII) and its type 1 receptor (AT1R) signaling. Here, we investigated the role of AngII/AT1R signal pathway in the resistance of IPC kidneys to subsequent I/R injury. IPC of kidneys was generated by 30 minutes of bilateral renal ischemia and 8 days of reperfusion. Sham-operation was performed to generate control (non-IPC) mice. To examine the roles of AngII and AT1R in IPC kidneys to subsequent I/R, IPC kidneys were subjected to either 30 minutes of bilateral kidney ischemia or sham-operation following treatment with AngII, losartan (AT1R blocker), or AngII plus losartan. IPC kidneys showed fibrotic changes, decreased AngII, and increased AT1R expression. I/R dramatically increased plasma creatinine concentrations in non-IPC mice, but not in IPC mice. AngII treatment in IPC mice resulted in enhancedmorphological damage, oxidative stress, and inflammatory responses, with functional impairment, whereas losartan treatment reversed these effects. However, AngII treatment in non-IPC mice did not change I/R-induced injury. AngII abolished the resistance of IPC kidneys to subsequent I/R via the enhancement of oxidative stress and inflammatory responses, suggesting that the AngII/AT1R signaling pathway is associated with
outcome in injury-experienced kidney.
Department
Dept. of Molecular Medicine (분자의학)
Publisher
School of Medicine
Citation
BioMed Research International, Vol.2014(null) : 1-10, 2014
Type
Article
ISSN
2314-6133
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35213
Authorize & License
  • AuthorizeOpen
Files in This Item:

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.