Abstract
The renin–angiotensin–aldosterone system (RAAS) is a key regulator of cardiovascular function. RAAS activity is upregulated in obesity despite concurrent renal sodium retention, which is a hallmark and principle determinant of obesity-associated hypertension. The contribution of adipose tissue to increased angiotensinogen and aldosterone plasma levels in obesity is probably due to the secretion of angiotensinogen and, as yet, unidentified aldosterone secretagogues by adipocytes. Increased circulating renin activity, on the other hand, is probably due to increased sympathetic activity in the obese. Modest weight reduction significantly reduces RAAS activity by uncertain mechanisms. Pharmacological blockade of the RAAS yielded promising results, both with regard to cardiovascular function and metabolic complications of obesity. These studies suggest that the activated RAAS is a prime pharmacological target for reducing the cardiometabolic risk in obese patients.
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