title: Angiotensin II removes kidney resistance conferred by ischemic preconditioning.
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 enhanced morphological 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.
authors.affiliation: Department of Anatomy and BK21 Plus Biomedical Convergence Program, Cardiovascular Research Institute, Kyungpook National University School of Medicine, 101 Dongin-dong Jung-gu, Daegu 700-422, Republic of Korea.
authors.forename: Hee-Seong
authors.identifier: 0000-0002-9620-351X
authors.initials: HS
authors.lastname: Jang
authors.affiliation: Department of Molecular Medicine and ODR Medical Research Center, Keimyung University School of Medicine, Daegu 704-701, Republic of Korea.
authors.forename: Jee In
authors.initials: JI
authors.lastname: Kim
authors.affiliation: Department of Anatomy, Jeju National University School of Medicine, Jeju 690-756, Republic of Korea.
authors.forename: Jinu
authors.identifier: 0000-0002-1313-4791
authors.initials: J
authors.lastname: Kim
authors.affiliation: School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu 702-701, Republic of Korea.
authors.forename: Jeen-Woo
authors.initials: JW
authors.lastname: Park
authors.affiliation: Department of Anatomy and BK21 Plus Biomedical Convergence Program, Cardiovascular Research Institute, Kyungpook National University School of Medicine, 101 Dongin-dong Jung-gu, Daegu 700-422, Republic of Korea.
authors.forename: Kwon Moo
authors.identifier: 0000-0002-1617-5919
authors.initials: KM
authors.lastname: Park
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D003404:Creatinine / Q000097:blood; D005355:Fibrosis; D019194:Ischemic Preconditioning / Q000379:methods*; D007668:Kidney / Q000473:pathology / Q000503:physiopathology; D007674:Kidney Diseases / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D003404:Creatinine