AT1R Blockade Inhibits Endothelial Dysfunction in Response to Mental Stress in Overweight/Obese Men

Acute exposure to mental stress (MS) leads to endothelial activation, microparticles release and, consequently, transient endothelial dysfunction in overweight/obesity grade 1 men. Considering that angiotensin II generates an oxidative imbalance mediated by angiotensin II type 1 receptors (AT1R), it is unknown whether this process is responsible for transient endothelial dysfunction present in MS in overweight/obesity grade 1. Therefore, the aim of this study was to determine endothelial responses to angiotensin II mediated by AT1R after MS in overweight/obesity grade I men. For this, fourteen overweight/obese men (27±7 years; 30.1±2.9 Kg/m2) participated in two randomized experimental sessions with oral administration of the AT1 receptor blocker (AT1R block) or placebo. Endothelial function was determined by flow-mediated dilation (FMD) before (baseline), 30 (30MS) and 60 (60MS) minutes after a five minute session of acute MS (Stroop Color Word Test). Blood samples (n=11) were obtained at before (baseline), during (MS) and 60 minutes (60MS) after MS for measurement of: endothelial microparticle (EMP, flow cytometry); endothelial progenitor cells (EPC, flow cytometry); nitrite (chemoluminescence); and oxidative stress [lipid peroxidation (TBARS), protein oxidation (carbonylated proteins) and antioxidant enzyme (catalase) by colorimetry]. During MS, heart rate, systolic, diastolic and mean blood pressure increased similarly in both conditions (p=0.01 vs. baseline). At the placebo session, FMD decreased significantly in 30MS (p=0.04 vs. baseline) and returned to baseline levels in 60MS (p=0.03 vs. 30MS). There was a significant increase in EPC in 60MS (p=0.04 vs. baseline). Carbonylated proteins (p=0.01 vs. baseline) and catalase activity increased during MS (p=0.02 vs. baseline) and returned to baseline in 60MS (p=0.01 vs. MS). No differences were observed in nitrite levels at the placebo session. At AT1R block session, FMD increased in 30MS (p =0.01 vs. baseline) and 60MS (p=0.02 vs. baseline), while EPC levels were different from placebo only 60MS (p=0.04 vs. placebo). There was a significant increase in nitrite (p=0.01 vs. baseline) while no change was observed in carbonylated proteins in 30MS and 60MS. Carbonylated protein concentration was lower during AT1R blockade in MS (p=0.04 vs. placebo). Catalase increased only in 60EM (p=0.02 vs. placebo). There were no differences in the concentrations of EMP and TBARS. In conclusion, AT1R blockade appears to increase flow-mediated dilatation and nitrite bioavailability in response to MS in addition to preventing the increase of protein oxidation after MS in overweight/obese men. Support or Funding Information Coordination for the Improvement of Higher Education Personnel (CAPES) Foundation for Research Support of the State of Rio de Janeiro (FAPERJ) National Council for Scientific and Technological Development (CNPq) This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.