16th World Cardiology Congress
Federal University of Espirito Santo, Brazil
Title: Aliskiren and L-arginine treatments restore ventricular hypertrophy and decrease oxidative stress in renovascular hypertension rats
Biography: Vinícius Mengal
Renovascular hypertension occurs by reduced renal perfusion pressure, which activates the renin-angiotensin-aldosterone system (RAAS). Several studies indicate that the increased angiotensin II and oxidative stress plays an important role in renovascular hypertension and progression of tissue damage. The purpose of this study was to test whether the administration of aliskiren (ALSK) and L-arginine (L-ARG) would restore ventricular hypertrophy and reduce oxidative stress in a rat renovascular hypertension model. Wistar rats underwent surgery for implantation of silver clip on the left renal artery to induce renovascular hypertension (2K1C). After 7 days was performed plethysmography of tail for indirect measurement of systolic blood pressure (SBP). The rats were divided in five groups: SHAM; 2K1C; 2K1C plus ALSK; 2K1C plus L-ARG; and 2K1C plus ALSK+ L-ARG. The treatment was performed for 21 days by gavage. At the end of treatment blood samples were taken and analyzed the dry weight of the left ventricle and the expression of SOD, CAT and gp91phox in the cardiac tissue by Western blotting. In addition, that the advanced oxidation product (AOPP) levels and the estimate of reactive oxygen species by dihydroethidium fluorescence were analyzed. After 21 days of treatment, only the ALSK+L-ARG group was effective in normalizing the arterial pressure (108.8±2.8 mm Hg). The L-ARG and ALSK+L-ARG groups did not show hypertrophy of the left ventricle. All treatments were effective in increase the antioxidant pathway and reduce oxidative pathway. In conclusion, the treatment with ALSK or L-ARG reduced oxidative stress and and reverse left ventricular hypertrophy.