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Abstract Background and Aims Renal ischemia/reperfusion injury is a common cause of acute kidney injury (AKI), and hypertension might contribute to the increased incidence of AKI. AKI has a multifactorial causality, but the mechanism of pathogenesis and the development of this disease are still incompletely defined. The purpose of this study was to compare the effects of AT1R blockade and AT2R simulation on AKI development in spontaneously hypertensive rats (SHR). Method We used male 24 weeks old SHR. Animals were divided into following experimental groups: sham operated rats (SHAM); rats with induced postischemic AKI (AKI); a group which received AT1R antagonist Losartan (10 mg/kg b.w.)(AKI+LOS) and group which received AT2R agonist novokinin (0.3 mg/kg b.w.)(AKI+NOVO) in the moment of kidney reperfusion. AKI was induced by surgical removal of right kidney followed by atraumatic clamp occlusion of the left renal artery for 40 minutes. Hemodynamic and biochemical measurements were done 24 hours after reperfusion. Results Conclusion Our results confirm the dominant role of AT1R on AKI development, but AT2R stimulation failed to buffer deleterious effects of AT1R hyperactivity on renal vasoconstriction and glomerular filtration. However, the role of AT2R during AKI development in hypertension will be in focus in our further studies.
Ivanov et al. (Wed,) studied this question.