Abstract
Rightfully considered as essential for hydro-electrolytic homeostasis, angiotensin II (Ang II) is the main product of the renin-angiotensin system (RAS). Ang II is one of the most important factors that contribute to the regulation of systemic arterial blood pressure (ABP). This major role is based on the effects exerted by RAS: Upon the kidney (RAS involvement in the control of salt and water excretion), upon the brain (RAS involvement in the control of water intake), and upon the sympathetic nervous system. It is currently known that there is a tight bidirectional link between high ABP and chronic kidney disease (CKD). Ang II causes vasoconstriction in the renal microvasculature, predominantly in the preglomerular arterioles. High ABP affects the target organs (eyes, brain, heart, kidneys) and it is known both as a cause and as an effect of CKD. Thus, there is a positive feedback mechanism that contributes even more to the increase in ABP and the progression of CKD. Along with its main hemodynamic effects, Ang II has direct proinflammatory actions, that also affect the structure and function of the kidney and heart. This study investigated the role of RAS and Ang II in the inflammation that accompanies the hypertension experimentally induced by Ang II in rats. Our data support the hypothesis that anti-inflammatory medication might alleviate the morphological and/or functional changes of the kidneys and heart that are related to Ang II-induced hypertension.