Effect of Losartan injection into paraventricular nucleus in renal ischemia-reperfusion injury
Mina Ranjbaran1, Behjat Seifi1, Mehri Kadkhodaee1 1 Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
Mina Ranjbaran, firstname.lastname@example.org
Aim: Acute kidney injury (AKI) still has a high mortality rate, despite the technical progress in managing it. The brain contains a tissue renin–angiotensin system, resulting in the local synthesis of Ang II within the brain. This study was designed to investigate whether microinjection of angiotensin II (Ang II) into the hypothalamicparaventricular nucleus (PVN) in renal ischemia–reperfusion (IR) injury has any effect on renal oxidative stress.
Method: Male Sprague–Dawley rats (250–300 g) were used. One week before the induction of left renal IR injury, right nephrectomy wasperformed 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 ofIR injury.
Ang II increased plasma creatinine, MDA levels and reduced SOD activity in the kidney compared with IR injury (p < 0.05).
Results: Ang II increased plasma creatinine, MDA levels and reduced SOD activity in the kidney compared with IR injury (p < 0.05).Losartan caused a reduction in plasma creatinineand renal MDA levels, and increased renal SOD activity compared with the IR group (p < 0.05).
Conclusion: These data demonstrated that microinjection of Ang II into the PVN, exaggeratedrenal IR injury by inducing oxidative stress in the kidney.
Key words: Angiotensin II, ischemia–reperfusion injury, paraventricular hypothalamic nucleus, oxidative stress