The physiological hydroelectrolytic balance and the redox steady state in the kidney are accomplished by an intricate interaction between signals from extrarenal and intrarenal sources and between antinatriuretic and natriuretic factors. Angiotensin II, atrial natriuretic peptide and intrarenal dopamine play a pivotal role in this interactive network. The balance between endogenous antioxidant agents like the renal dopaminergic system and atrial natriuretic peptide, by one side, and the prooxidant effect of the renin angiotensin system, by the other side, contributes to ensuring the normal function of the kidney. Different pathological scenarios, as nephrotic syndrome and hypertension, where renal sodium excretion is altered, are associated with an impaired interaction between two natriuretic systems as the renal dopaminergic system and atrial natriuretic peptide that may be involved in the pathogenesis of renal diseases. The aim of this review is to update and comment the most recent evidences about the intracellular pathways involved in the relationship between endogenous antioxidant agents like the renal dopaminergic system and atrial natriuretic peptide and the prooxidant effect of the renin angiotensin system in the pathogenesis of renal inflammation. 1. Introduction A normal redox state of cells depends on a delicate balance between oxidative species and antioxidant mechanisms. Acting as cellular messengers, reactive oxygen species (ROS) are involved in the destruction of invading pathogens [1]. Chronic inflammatory conditions such as atherosclerosis or hypertension can alter the normal redox state of the cells through an overproduction of free radicals that leads to an increase in oxidative stress with disruption of the normal cellular signaling mechanisms [2–5]. In the kidney, oxidative stress and infiltration of inflammatory cells represent key factors for the development of renal injury and hypertension [6]. Angiotensin II (Ang II) that displays hypertensive and prooxidant properties, by one side, and the atrial natriuretic peptide (ANP) and renal dopamine, by the other side, both with hypotensive and antioxidant properties, are local factors closely related to the development and progression of glomerular and tubular injury [7, 8]. 2. Renin-Angiotensin System and Renal Oxidative Stress Ang II mediates most of the renin angiotensin system (RAS) effects through activation of two types of receptors: Ang II type 1 (AT1R) and Ang II type 2 (AT2R). In the last decades, novel components of the RAS have been recognized, including the (pro) renin
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