Laboratório de Ciências do Exercício, Departamento de Fisiologia e Farmacologia, Universidade Federal Fluminense, Niterói, RJ, Brasil.
Instituto Nacional de Ciência e Tecnologia - (In)Atividade Física e Exercício, Conselho Nacional de Desenvolvimento Científico e Tecnológico, Universidade Federal Fluminense, Niterói, RJ, Brasil.
Braz J Med Biol Res. 2023 Mar 24;56:e12547. doi: 10.1590/1414-431X2023e12547. eCollection 2023.
The main goal of this study was to determine whether oxidative imbalance mediated by AT1 receptor (AT1R) is responsible for deleterious endothelial responses to mental stress (MS) in overweight/obese class I men. Fifteen overweight/obese men (27±7 years old; 29.8±2.6 kg/m2) participated in three randomized experimental sessions with oral administration of the AT1R blocker olmesartan (40 mg; AT1R blockade) or ascorbic acid (AA; 3g) infusion or placebo [both intravenously (0.9% NaCl) and orally]. After two hours, endothelial function was determined by flow-mediated dilation (FMD) before (baseline), 30 min (30MS), and 60 min (60MS) after a five-minute acute MS session (Stroop Color Word Test). Blood was collected before (baseline), during MS, and 60 min after MS for redox homeostasis profiling: lipid peroxidation (TBARS; thiobarbituric acid reactive species), protein carbonylation, and catalase activity by colorimetry and superoxide dismutase (SOD) activity by an ELISA kit. At the placebo session, FMD significantly decreased 30MS (P=0.05). When compared to baseline, TBARS (P<0.02), protein carbonylation (P<0.01), catalase (P<0.01), and SOD (P<0.01) increased during the placebo session. During AT1R blockade, FMD increased 30 min after MS (P=0.01 vs baseline; P<0.01 vs placebo), while AA infusion increased FMD only 60 min after MS. No differences were observed during MS with the AT1R blockade and AA regarding TBARS, protein carbonylation, catalase, and SOD. AT1R-mediated redox imbalances played an important role in endothelial dysfunction to mental stress.
本研究的主要目的是确定血管紧张素受体（AT1R）介导的氧化失衡是否是超重/肥胖 I 级男性精神应激（MS）导致内皮功能障碍的原因。15 名超重/肥胖男性（27±7 岁；29.8±2.6 kg/m2）参与了三项随机实验，分别给予 AT1R 阻滞剂奥美沙坦（40mg；AT1R 阻断）、抗坏血酸（AA；3g）输注或安慰剂[静脉内（0.9%NaCl）和口服]。两小时后，在急性 MS 5 分钟后（Stroop 颜色字测试），通过血流介导的扩张（FMD）测定内皮功能，在（基线）之前、30 分钟（30MS）和 60 分钟（60MS）后。在（基线）之前、MS 期间和 MS 后 60 分钟收集血液，用于氧化还原平衡谱分析：脂质过氧化（TBARS；硫代巴比妥酸反应性物质）、蛋白羰基化和比色法测定的过氧化氢酶活性以及 ELISA 试剂盒测定的超氧化物歧化酶（SOD）活性。在安慰剂阶段，FMD 在 30MS 时显著降低（P=0.05）。与基线相比，TBARS（P<0.02）、蛋白羰基化（P<0.01）、过氧化氢酶（P<0.01）和 SOD（P<0.01）在安慰剂阶段增加。在 AT1R 阻断时，MS 后 30 分钟 FMD 增加（P=0.01 与基线相比；P<0.01 与安慰剂相比），而 AA 输注仅在 MS 后 60 分钟增加 FMD。在 AT1R 阻断和 AA 期间，MS 期间没有观察到 TBARS、蛋白羰基化、过氧化氢酶和 SOD 之间的差异。AT1R 介导的氧化还原失衡在精神应激导致内皮功能障碍中起重要作用。
