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Renin-angiotensin system (RAS) is activated during ischemic acute kidney injury. Via AT2R, angiotensin II, promotes vasodilatory, anti-inflammatory and antifibrotic actions and participates in tissue repair. We previously described that 40 min of renal ischemia followed by 1 day of reperfusion in male rats induced severe tissue damage and a decrease in glomerular filtration rate (GFR) that were partially prevented with a high dose of the AT2R agonist, C21 (1 mg/kg/day). Sex differences in the development of renal ischemia-reperfusion (IR) injury and in RAS components expression have been reported.
Fussi et al. (Mon,) studied this question.