The renin‑angiotensin‑aldosteron system (RAAS) is a hormonal system that contributes to regulation of blood pressure and volume of extracellular fluids, in both normotensive and hypertensive individuals. Hypertension affects the target organs (kidneys) and leads to a vicious circle that contributes to maintaining a high arterial pressure. Besides the hemodynamic effects of RAAS/Ang II, Ang II has direct impact on structure/function of kidneys, leading to renal injury. Recently, the proinflammatory effect of Ang II has been discovered. Low renal inflammation determined by excessive circulating RAAS, mostly at renal level, promotes and continues the renal disease. This review presents the inflammatory mechanisms initiated by Ang II at renal level, which induce development of renal injury. Identification of such mechanisms might lead to the discovery of new therapeutic approaches for hypertension/target organs damage.