Brain renin-angiotensin system blockade with orally active aminopeptidase A inhibitor prevents cardiac dysfunction after myocardial infarction in mice

Brain renin-angiotensin system (RAS) hyperactivity has been implicated in sympathetic hyperactivity and progressive left ventricular (LV) dysfunction after myocardial infarction (MI). Angiotensin III, generated by aminopeptidase A (APA), is one of the main effector peptides of the brain RAS in the control of cardiac function. We hypothesized that orally administered firibastat (previously named RB150), an APA inhibitor prodrug, would attenuate heart failure (HF) development after MI in mice, by blocking brain RAS hyperactivity.

Source: Journal of Molecular and Cellular Cardiology - December 29, 2018 Category: Cytology Authors: Sol ène Emmanuelle Boitard, Yannick Marc, Mathilde Keck, Nathalie Mougenot, Onnik Agbulut, Fabrice Balavoine, Catherine Llorens-Cortes Source Type: research