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Aldosterone is part of the renin–angiotensin–aldosterone system. It has a plasma half-life of less than 20 minutes. [ 9 ] 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 ...
The name mineralocorticoid derives from early observations that these hormones were involved in the retention of sodium, a mineral.The primary endogenous mineralocorticoid is aldosterone, although a number of other endogenous hormones (including progesterone [1] and deoxycorticosterone) have mineralocorticoid function.
Antimineralocorticoid mechanism of action. Aldosterone is a mineralocorticoid which is synthesized in the adrenal glands. [5] When aldosterone is secreted from the adrenal glands, it binds to the mineralocorticoid receptor in the renal tubule cell and forms a complex. [6]
The mineralocorticoid receptor (or MR, MLR, MCR), also known as the aldosterone receptor or nuclear receptor subfamily 3, group C, member 2, (NR3C2) is a protein that in humans is encoded by the NR3C2 gene that is located on chromosome 4q31.1-31.2. [5] MR is a receptor with equal affinity for mineralocorticoids and glucocorticoids.
The outermost layer, the zona glomerulosa is the main site for the production of aldosterone, a mineralocorticoid. The synthesis and secretion of aldosterone are mainly regulated by the renin–angiotensin–aldosterone system. The zona glomerulosa cells express a specific enzyme aldosterone synthase (also known as CYP11B2).
Aldosterone binds to aldosterone receptors (mineralocorticoid receptors) increasing sodium reabsorption in an effort to increase blood pressure and improve fluid status in the body. When excessive sodium reabsorption occurs, there is an increasing loss of K + in the urine and can lead to clinically significant decreases, termed hypokalemia .
Another mechanism proposed by RW Schrier [6] suggests that aldosterone involves synergistic processes. In addition to increasing renal perfusion pressure, the resultant volume expansion decreases proximal sodium reabsorption and increases sodium delivery to the distal nephron sites of mineralocorticoid action.
The renin–angiotensin–aldosterone system is a major blood pressure regulating mechanism. Markers of electrolyte and water imbalance in the body such as hypotension , low distal tubule sodium concentration, decreased blood volume and high sympathetic tone trigger the release of the enzyme renin from the cells of juxtaglomerular apparatus in ...