Role of the Renin-Angiotensin System and Aldosterone on Cardiometabolic Syndrome

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.

Adipokines and cardiovascular disease: A comprehensive review

“…1) (ref. 19 ). In summary, increased amount of visceral adipose tissue induces production of aldosterone and glucocorticoids, and these hormones in turn facilitate the development of chronic inflammation in adipose tissue with subsequent overproduction of harmful adipokines (Fig.…”

“…Blockade of the renin-angiotensinaldosterone system with ACE inhibitors, AT1-blockers or spironolactone is one of the basic approaches in the treatment of hypertension, congestive heart failure and coronary artery disease. Some studies suggest that mineralocorticoid receptors in adipocytes promote the expression of inflammatory adipokines and facilitate the effect of the pro-adipogenic effect of aldosterone and glucocorticoids 19 . Inhibition of these receptors in experimental studies decreases the expression of pro-inflammatory factors in adipose tissue and increases the expression of adiponectin in heart and adipose tissue 19 .…”

“…Some studies suggest that mineralocorticoid receptors in adipocytes promote the expression of inflammatory adipokines and facilitate the effect of the pro-adipogenic effect of aldosterone and glucocorticoids 19 . Inhibition of these receptors in experimental studies decreases the expression of pro-inflammatory factors in adipose tissue and increases the expression of adiponectin in heart and adipose tissue 19 . Adipose tissue produces an as yet unidentified mineralocorticoid releasing factor which stimulates the production of aldosterone and glucocorticoids (please see Fig.…”

Asociación y efectos de interacción en los genes AGT, AGTR1, ACE, ADRB2, DRD1, ADD1, ADD2, ATP2B1, TBXA2R y PTGS2 sobre la hipertensión en población antioqueña

“…Los principales sistemas fisiológicos que se encuentran involucrados en el control de la presión arterial son el sistema renina-angiotensina-aldosterona, el endotelio vascular, la transducción de señales por vía del sistema nervioso y las proteínas del citoesqueleto, que se encargan del mantenimiento del flujo sanguíneo (presión sanguínea y volumen de fluidos extracelulares en el cuerpo), mediación de reacciones de vasodilatación-vasoconstricción y la regulación de la concentración de sales (27)(28)(29)(30)(31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43)(44).…”

Increased aldosterone in patients with metabolic syndrome; an additional risk factor

“…Many recent studies involve aldosterone in the pathogenesis of the cardiometabolic syndrome [2,4,5], although this relationship is complex and not well established, there is some evidence that different factors could act on it such as insulin resistance, renin-angiotensinaldosterone system, oxidative stress, sodium retention and volume overload, increased sympathetic activity, levels of free fatty acids, or inflammatory cytokines and adipokines [5].…”