Tehran University Medical Journal

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Background: In a recent study, we were able to demonstrate a role for leukocyte transfer in the induction of liver damage in recipient mice after induction of IR (60 min of bilateral renal artery occlusion and 3 hrs reperfusion) injury in donors. The present study investigates the role of leukocyte transfer in the induction of kidney damage in recipient mice after induction of renal IR injury in donors.

Methods: Mice were divided into two sham and renal IR groups. After anesthesia, leukocytes were isolated from blood and were transferred to the two recipient groups: the intact recipient mice received leukocytes from the sham donor group (Sham recipient) and the intact recipient mice that received leukocytes from IR donor group (IR recipient). After 24 hrs, the recipient mice were anesthetized and blood samples and renal tissues were collected.

Results: Renal malondialdehyde (MDA) increased and glutathione and superoxide dismutase (SOD) decreased significantly in IR recipient group in comparison to sham recipient group. Although renal function tests, including BUN and plasma creatinine were significantly different between IR donor and sham donor groups, but they were not significantly different in two recipient groups. Renal tissues in IR donor group showed extensive damage compared to sham group, but in IR recipients' kidneys, they were different from IR donor tissues despite being different from their respective sham group.

Conclusion: These findings are suggestive of implication of leukocytes in renal tissue damage and oxidative stress after renal IR injury.

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Background: The renal sympathetic nerve activity (RSNA) is enhanced in renal failure. Paraventricular nucleus in hypothalamus is an important central site to regulate sympathetic activity. There are angiotensin II (Ang) II receptors in this nucleus. The aim of this study was to evaluate the effects of angiotensin II in hypothalamic paraventricular nucleus (PVN) on renal ischemia-reperfusion injury and RSNA. Methods: This study was done at 2013 in Physiology department of Tehran University of Medical Sciences. One week before the induction of renal Ischemia-Reperfusion (IR) in Sprague-Dawley rats, a cannula was inserted into the right PVN for microinjection of different doses of Ang II (3, 30, and 300 ng). Then right nephrectomy was done. After one week recovery, renal IR injury was induced by clamping the left renal artery for 45 minute and then reperfusion for 3 or 24 hour. Ten minutes before the induction of renal ischemia-reperfusion, administration of different doses of angiotensin II were done in different groups. In all animals, left renal sympathetic activity was recorded before and during renal ischemia. After 3 or 24 hours reperfusion the blood, kidney and brain were collected to assay renal function and histology and oxidative stress indices Superoxide Dismutase, SOD and Malondialdehyde, MDA) in PVN. Results: Administration of different pharmacological doses of angiotensin II into PVN exaggerated the renal IR injury. Angiotensin II in different doses increased the plasma creatinine and BUN levels and renal histological markers in comparison to renal IR in-jury (P<0.05). Angiotensin II had detrimental effects on RSNA and oxidative stress in-dices Super Oxide Dismutase (SOD) and Malondialdehyde (MDA) in PVN as the dose was increased (P<0.05). Conclusion: These data showed that the PVN is a responsive site for central Ang II-induced damage in renal IR injury. We suggested the central effects of Ang II in the PVN on renal IR injury are mediated by oxidative stress in the PVN, and the peripheral effects by a sympathetic pathway.