THE ROLE OF ALDOSTERONE EXCESS IN THE DEVELOPMENT OF CARDIOVASCULAR AND METABOLIC DISORDERS

Aldosterone is a mineralocorticoid hormone produced by the zona glomerulosa of the adrenal cortex and plays an essential role in sodium balance, potassium homeostasis, extracellular fluid volume, and blood pressure regulation. Excessive aldosterone secretion can lead to significant cardiovascular, renal, and metabolic disturbances. The aim of this study was to analyze the pathophysiological mechanisms and clinical consequences of aldosterone excess, with particular attention to primary aldosteronism. A literature-based analytical approach was used to evaluate the renin-angiotensin-aldosterone system, mineralocorticoid receptor signaling, renal sodium reabsorption, potassium excretion, vascular remodeling, myocardial fibrosis, insulin resistance, and diagnostic principles. The analysis indicates that chronic aldosterone excess promotes sodium retention, volume expansion, hypertension, hypokalemia, endothelial dysfunction, vascular stiffness, left ventricular hypertrophy, myocardial fibrosis, and increased cardiovascular risk. Aldosterone may also contribute to metabolic abnormalities through oxidative stress, inflammation, and impaired insulin signaling. Primary aldosteronism is now recognized as one of the most important potentially treatable causes of secondary hypertension. Accurate diagnosis requires appropriate screening using the aldosterone-to-renin ratio, confirmatory testing where indicated, adrenal imaging, and subtype evaluation. Treatment with mineralocorticoid receptor antagonists or adrenal surgery can significantly reduce cardiovascular risk. Understanding aldosterone biology is therefore essential for modern endocrine and cardiovascular medicine.