An antioxidant treatment is able to prevent hypertension and the imbalance of the renin angiotensin system induced by a high sodium diet.?

KOUYOUMDZIAN, N.M.; CAO, G.; PENNA, S L DELLA; SUSANA GORZALCZANIC; NATALIA L RUKAVINA MIKUSIC; CHOI, M.R.; MARCELA PANDOLFO; FERNÁNDEZ, B.E.; JORGE E TOBLLI; ROSON MI

Congreso; III International Congress in Translational Medicine Facultad de Farmacia y Bioquímica,; 2016

BACKGROUND. Salt sensitivity, which is responsible for the increase of blood presure in response to a high salt intake, is a risk factor for cardiovascular disease and mortality. Current dietary intake of salt in western societies is a determinant factor for the genesis of hypertension and may even cause blood pressure-independent target organ damage, including the kidney.The aim of this study was to determine the effects of a high salt diet administered to normal rats on blood pressure and on the balance between antagonist components of the renal renin-angiotensin system in the kidney, and to evaluate the preventive action of antioxidant treatment with tempol. METHODS. Male Sprague-Dawley rats were fed with 8% NaCl (high-salt group, HS) or 0.4% NaCl (normal-salt group, NS) diet for 3 weeks, with or without tempol (T) (1 mM, administered in drinking water). Mean arterial pressure (MAP), glomerular filtration rate (GFR), urinary sodium excretion (UVNa) and fractional sodium excretion (FENa) were measured. We evaluated Angiotensin II (Ang II), Angiotensin 1-7 (Ang 1-7), Angiotensin Converting Enzyme 2 (ACE2), Mas Receptor (MasR), Angiotensin Type 1 Receptor (AT1R) and Angiotensin Type 2 Receptor (AT2R) immunoexpression in renal tissues by immunohistochemistry. Immunostaining was evaluated by Image Pro Plus software analysis and expressed as integrated optical density (IOD) ± SEM in renal tissue. All values are mean ± SEM (n= 5-6 per group).CONCLUSION These findings suggest that a high salt diet leads to alter the homeostasis and balance between opposing components of the renal RAS by favouring the increase of local synthesis of hypertensive factors of the renal RAS in tubule cells and by inhibiting the renal expression of antihipertensive factors of the RAS. This imbalance is responsible for the development of oxidative stress and inflammation in renal tubulointersticial tissues and hypertension, which can be prevented or restored by chronic antioxidant treatment with tempol, favouring the natriuretic action of antihipertensive components of the renal RAS.