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Central angiotensin‐converting enzyme 2 overexpression normalizes angiotensin II type I and type II receptor expression in mouse brain stem during chronic heart failure

In chronic heart failure (CHF), changes in angiotensin II type I receptor (AT1R) and type II receptor (AT2R) expression in the brain are associated with increased sympathetic outflow which contributes to the progressive deterioration of cardiac function. We hypothesized that central ACE2 overexpression normalizes AT1R and AT2R expression in the brain stem in CHF. Samples of nucleus tractus solitaries (NTS) and rostral ventrolateral medulla (RVLM) were punched from wild type (WT) and syn‐hACE2 (SA) transgenic mice after 4‐week myocardial infarction or sham surgery. Receptor protein was measured by Western blotting. The localizations of AT1R and AT2R were confirmed by immunofluorescence. AT1R expression was up‐regulated in both NTS (0.16±0.04 vs. WT sham 0.05±0.004, p<0.05) and RVLM (0.11±0.004 vs. WT sham 0.07±0.01, p<0.005) in WT CHF mice. This up‐regulation was attenuated in SA CHF mice in RVLM (0.05±0.001 vs. WT CHF, p<0.05) and a trend for down regulation was observed in the NTS (0.07±0.01 vs. WT CHF, p=0.10). AT2R expression in NTS was decreased in WT CHF mice (0.20±0.03 vs. WT sham 0.35±0.02, p<0.005). This decrease was normalized in SA CHF animals (0.29±0.02 vs. WT CHF, p<0.005). No significant change was seen for AT2R expression in RVLM. This study suggests that ACE2 overexpression normalizes the expression of central angiotensin receptors, and thereby may contribute to restore the autonomic function in CHF.