AAS administration in male Wistar rats has been found to alter inflammatory cytokines and angiotensin-converting enzyme (ACE) activity, disrupting the Bezold–Jarisch reflex and leading to hypertension and subsequent cardiac hypertrophy ases ACE levels, resulting in elevated angiotensin II and activation of the AT-1 receptor, which induces myocardial hypertrophy and fibrosis independent of blood pressure (51). This evidence concerns the gene AGT and cardiac hypertrophy.