Abstract P152: Exercise Training Upregulates Nrf2 Gene Expression in the RVLM of Mice With Heart failure

• Published in: Hypertension (Dallas, Tex. 1979) Tex. 1979), 2018-09, Vol.72 (Suppl_1)
• Main Authors: Wafi, Ahmed M, Gao, Lie, Yu, Li, Zucker, Irving H
• Format: Article
• Language: English
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/hyp.72.suppl_1.P152

Abstract only Sympatho-excitation is an important hallmark in the heart failure (HF) state. It is known that HF is associated with global oxidative stress, which contributes to pathogenesis of sympatho-excitation. Central reactive oxygen species (ROS) accumulate within neurons and evoke alterations in protein function, leading to an enhanced neuronal excitability, thereby evoking the higher level of sympathetic activation in HF. On the other hand, exercise training (ExT) is associated with a reduction of oxidative stress, in part by upregulation of antioxidant enzymes. However, the link between ExT and antioxidants in the brain of animals with HF has not been explored. In this study, we hypothesized ExT enhances transcriptional activation of Nuclear factor (erythroid-derived 2)-like 2 (Nrf2), a master transcription factor that modulates a wide array of antioxidant enzyme gene expression, in the rostral ventrolateral medulla (RVLM). Sham and coronary artery ligation-induced HF mice were divided into either sedentary (Sed) or ExT groups. After 6 weeks of treadmill training, maximal exercise tolerance, urinary norepinephrine (NE) and Nrf2 as well as NAD(P)H dehydrogenase [quinone] 1 (NQO1) gene expression were evaluated by real time RT-PCR. We found that: (1) HF mice displayed significantly lower maximal distance than Sham mice, which was improved by ExT (maximal distance: Sham- Sed 255 ± 34 m (n = 6), HF Sed 148 ± 37 (n = 5), HF ExT 304 ± 34 (n = 6), p