title: Enhancement of renal oxidative stress by injection of angiotensin II into the paraventricular nucleus in renal ischemia-reperfusion injury.
abstract: This study was designed to investigate whether microinjection of angiotensin II (Ang II) into the hypothalamic paraventricular nucleus (PVN) in renal ischemia-reperfusion (IR) injury has any effect on renal oxidative stress and damage through renal sympathetic nerve activity (RSNA). One week before the induction of left renal IR injury, right nephrectomy was performed and a cannula was placed into the right PVN. Rats were then distributed among 4 groups (n = 6); Sham, IR, IR + Ang II, and IR + Ang II + losartan. Renal IR injury was induced by clamping the left renal artery for 45 min followed by 24 h reperfusion. Losartan (0.3 μg) and Ang II (3 ng) were microinjected into the PVN at 20 min and 10 min, respectively, before the induction of IR injury. Ang II increased plasma creatinine, urinary NAG activity, and histological changes, and enhanced RSNA compared with the IR group (p < 0.05). Ang II increased malondialdehyde (MDA) levels and reduced superoxide dismutase (SOD) activity in the kidney compared with IR injury. Losartan caused a reduction in plasma creatinine, urinary NAG activity, histological changes, renal sympathetic nerve activity (RSNA), and renal MDA levels, and increased renal SOD activity compared with the IR group (p < 0.05). These data demonstrated that increased RSNA activity, via microinjection of Ang II into the PVN, exaggerated renal IR injury by inducing oxidative stress in the kidney.
authors.affiliation: a Department of Physiology, Faculty of Medicine, Tehran University of Medical Sciences, Tehran 14155-6447, Iran.
authors.forename: Behjat
authors.initials: B
authors.lastname: Seifi
authors.forename: Mehri
authors.initials: M
authors.lastname: Kadkhodaee
authors.forename: Enayatollah
authors.initials: E
authors.lastname: Bakhshi
authors.forename: Mina
authors.initials: M
authors.lastname: Ranjbaran
authors.forename: Parisa
authors.initials: P
authors.lastname: Ahghari
authors.forename: Tayebeh
authors.initials: T
authors.lastname: Rastegar
mesh_terms: D000118:Acetylglucosaminidase / Q000652:urine; D000804:Angiotensin II / Q000494:pharmacology / Q000502:physiology*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D003404:Creatinine / Q000097:blood; D007668:Kidney / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D019808:Losartan / Q000494:pharmacology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008845:Microinjections; D018384:Oxidative Stress / Q000187:drug effects*; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects* / Q000503:physiopathology; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D017382:Reactive Oxygen Species; D000804:Angiotensin II; D008315:Malondialdehyde; D003404:Creatinine; D013482:Superoxide Dismutase; D000118:Acetylglucosaminidase; D019808:Losartan
keywords: angiotensin II; angiotensine II; hypothalamic paraventricular nucleus; ischemia–reperfusion; ischémie reperfusion; kidney; noyau para-ventriculaire de l’hypothalamus; oxidative stress; rein; stress oxidant