Angiotensin II in paraventricular nucleus is exaggerated the renal ischemia-reperfusion injury

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. 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. 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 injury (P<0. 05). Angiotensin II had detrimental effects on RSNA and oxidative stress indices Super Oxide Dismutase (SOD) and Malondialdehyde (MDA) in PVN as the dose was increased (P<0. 05). 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.