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BioMed Research International
Volume 2014, Article ID 512619, 8 pages
Research Article

Acute Superoxide Radical Scavenging Reduces Blood Pressure but Does Not Influence Kidney Function in Hypertensive Rats with Postischemic Kidney Injury

1Department of Cardiovascular Physiology, Institute for Medical Research, University of Belgrade, 11129 Belgrade, Serbia
2Institute of Pathology, Medical School, University of Belgrade, 11129 Belgrade, Serbia

Received 4 February 2014; Revised 16 May 2014; Accepted 19 May 2014; Published 22 June 2014

Academic Editor: Emmanuel A. Burdmann

Copyright © 2014 Zoran Miloradović et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Acute kidney injury (AKI) is associated with significant morbidity and mortality in hypertensive surroundings. We investigated superoxide radical molecules influence on systemic haemodynamic and kidney function in spontaneously hypertensive rats (SHR) with induced postischemic AKI. Experiment was performed in anesthetized adult male SHR. The right kidney was removed, and left renal artery was subjected to ischemia by clamping for 40 minutes. The treated group received synthetic superoxide dismutase mimetic TEMPOL in the femoral vein 5 minutes before, during, and 175 minutes after the period of reperfusion, while the control AKI group received the vehicle via the same route. All parameters were measured 24 h after renal reperfusion. TEMPOL treatment significantly decreased mean arterial pressure and total peripheral resistance compared to AKI control. It also increased cardiac output and catalase activity . Lipid peroxidation and renal vascular resistance were decreased in TEMPOL . Plasma creatinine and kidney morphological parameters were unchanged among TEMPOL treated and control groups. Our study shows that superoxide radicals participate in haemodynamic control, but acute superoxide scavenging is ineffective in glomerular and tubular improvement, probably due to hypertension-induced strong endothelial dysfunction which neutralizes beneficial effects of scavenging.