![]() Aldosterone can exert its functions through its interaction with the mineralocorticoid receptor (MR). In fact, excess aldosterone induces vascular stiffness, thrombosis, and left ventricular remodeling, and enhances mortality rate. Especially, vascular and structural changes in the heart are reported to increase the risk of cardiovascular disease and mortality. These altered mechanisms are related to each other and cause metabolic abnormality, coronary artery disease (CAD), and renal dysfunction. The excess of aldosterone induces pathophysiological alterations such as exacerbated inflammation, oxidative stress, and fibrosis. We also describe the risk of cardiovascular events and renal dysfunction in hyperaldosteronism. In this review, we focus on currently available evidence regarding the role of aldosterone in alterations of the cardiovascular and renal systems. Therefore, understanding the effects of aldosterone on the body is important for health maintenance in hypertensive patients. Thus, aldosterone affects several tissues, especially in the cardiovascular system, and the metabolic and pathophysiological alterations are related to severe diseases. These alterations can result in coronary artery disease, including ischemia and myocardial infarction, left ventricular hypertrophy, heart failure, arterial fibrillation, intracarotid intima thickening, cerebrovascular disease, and chronic kidney disease. Excess aldosterone can lead to harmful metabolic and other pathophysiological alterations, as well as cause inflammatory, oxidative, and fibrotic effects in the heart, kidney, and blood vessels. ![]() Primary aldosteronism is associated with an increased risk of cardiovascular disease and kidney dysfunction compared to essential hypertension. The excess of aldosterone, also known as primary aldosteronism, is the most common secondary cause of hypertension. Aldosterone, a vital hormone of the human body, has various pathophysiological roles. ![]()
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