AA attenuated hemodynamic alterations (high blood pressure, heart rate, hind limb vascular resistance, and low hind limb blood flow), RAS activation (increased angiotensin II and angiotensin-converting enzyme activity in blood with enhanced AT1R and suppressed AT2R expression), oxidative stress (low levels of nitric oxide metabolites with increased generation of superoxide, MDA, and upregulation of gp91phox protein expression), and inflammation (increased TNF-α, NF-κB, and p-NF-κB expressions) in renal hypertensive 2K-1C rats. Here, ACE is linked to renal hypertension.