Abstract
Aldosterone facilitates cardiovascular damage by increasing blood pressure and through different mechanisms that are independent of its effects on blood pressure. In this respect, recent evidence involves aldosterone in the pathogenesis of metabolic syndrome. Although this relationship is complex, there is some evidence suggesting that different factors may play an important role, such as insulin resistance, renin-angiotensin-aldosterone system, oxidative stress, sodium retention, increased sympathetic activity, levels of free fatty acids, or inflammatory cytokines and adipokines. In addition to the classical pathway by which aldosterone acts through the mineralocorticoid receptors leading to sodium retention, aldosterone also has other mechanisms that influence cardiovascular tissue remodelling. Finally, overweight and obesity promote the adrenal secretion of aldosterone, increasing the predisposition to type 2 diabetes mellitus. Further studies are needed to better establish therapeutic strategies that act on the blockade of mineralocorticoid receptor in the treatment and prevention of cardiovascular diseases related to the excess of aldosterone and the metabolic syndrome.
Highlights
Prevalence of hypertension and obesity is increasing around the world, and data from NHANES III show that hypertension increases parallel to a rising body mass index [1]
Most studies link abdominal obesity and cardiometabolic disorders with the inflammatory status and oxidative stress that lead to the development of insulin resistance [4, 5]
Hypertension usually occurs at the same time with other risk factors: insulin resistance, central obesity, dyslipidemia, and carbohydrate disorders, to constitute the so-called cardiometabolic syndrome
Summary
Prevalence of hypertension and obesity is increasing around the world, and data from NHANES III show that hypertension increases parallel to a rising body mass index [1]. In association with obesity and insulin resistance, promote nongenomic inflammation and oxidative stress, which advance the development of resistant hypertension through a number of mechanisms [9] In this way, it has been demonstrated that aldosterone can inhibit the endothelium-dependent relaxation by decreasing nitric oxide bioavailability (a consequence of increased reactive oxygen species generation). Perivascular fibrosis induced by aldosterone reduces vascular compliance and increases arterial stiffness, and an increased Na/H interchange stimulates vascular smooth muscle cell proliferation [25, 26] These actions potentiate the elevation of blood pressure levels that occurs as consequence of classical effects of aldosterone (salt retention and volume expansion), causing severe hypertension that is resistant to treatment unless an appropriate mineralocorticoid receptor antagonist (such as spironolactone or eplerenone) is used as part of the therapeutic strategy
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