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Exercise training normalizes ACE and ACE2 in the brain of rabbits with pacing induced chronic heart failure

Activation of the renin‐angiotensin system (RAS) in the brain plays a critical role in sympatho‐excitation of chronic heart failure (CHF). Exercise training (EX) normalizes sympathetic outflow. The mechanisms that regulate angiotensin converting enzyme (ACE) in the brain and the effect of EX on ACE are unknown. The aim of this study was to investigate the regulation of ACE and ACE2, a homologue of ACE, in various areas of the brain with a pacing CHF‐EX model. Experiments were performed on four groups of New Zealand White rabbits: sham, sham + EX, CHF, and CHF + EX (n=5/group). Punches of the PVN, NTS, and RVLM (n=2/group) were also measured. Western blot analysis and double immunofluoresence were performed to measure and localize expression of ACE and ACE2. ACE expression in the cerebellum, medulla, and hypothalamus was significantly higher in CHF rabbits compared to sham (1.0±0.2 to 2.2±0.1 in the hypothalamus, P<0.05). EX normalized this upregulation compared to CHF (0.5±0.1 to 2.2±0.1 in the hypothalamus). ACE2 was significantly decreased in CHF. EX normalized ACE2 in the PVN, NTS, and RVLM (0.03±0.02 CHF to 0.8±0.3 CHF + EX in the RVLM). ACE was present in both endothelial cells and neurons. The results suggest that EX normalizes ACE and ACE2 in sympatho‐regulatory areas.