The net effect of these drugs is to reduce sodium and water retention but increase the retention of potassium. Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives, like lisinopril, which lowers blood pressure by blocking the angiotensin-converting enzyme (ACE), leading to lower aldosterone secretion. It has a plasma half-life of less than 20 minutes. Īldosterone is part of the renin–angiotensin–aldosterone system. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure, and blood volume. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na +), and potassium (K +) levels. It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland.

Adrenal gland hormone synthesis