Does Renin‐Angiotensin‐Aldosterone System Inhibition Impact Obesity as a Co–Risk Factor?

Obesity is an independent risk factor for cardiovascular disease (CVD).  When combined with smoking, diabetes, and hypertension (HTN), obesity has a synergistic effect to increase CVD risk 21‐fold.  Obesity damages multiple target organs, which are targets of “angry fat”, to increase risk of diabetes and fatty liver.  Many of these effects are due to ectopic fat deposition, increased oxidative stress, and inflammation. Importantly, the adipocyte is a source of angiotensinogen, potentially leading to renin‐angiotensinogen‐aldosterone system (RAAS) activation and HTN, which is 3‐fold more prevalent in obese compared with nonobese populations.  Emerging evidence suggests that the RAAS may also play a role in metabolism and the complications of obesity. Further research is needed to determine whether RAAS modulation with angiotensin receptor blockers will be useful not only for treating obesity‐associated HTN, but also for the metabolic and other complications of obesity, particularly by reducing damage from oxidative stress.

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