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(ăl'dōstĭrōn`), steroid secreted by the cortex of the adrenal gland. It is the most potent hormonehormone,
secretory substance carried from one gland or organ of the body via the bloodstream to more or less specific tissues, where it exerts some influence upon the metabolism of the target tissue.
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 regulating the body's electrolyte balance. Aldosterone acts directly on the kidney to decrease the rate of sodium-ion excretion (with accompanying retention of water), and to increase the rate of potassium-ion excretion. The secretion of aldosterone appears to be regulated by two mechanisms. First, the concentration of sodium ions may be a factor since increased rates of aldosterone secretion are found when dietary sodium is severely limited. Second, reduced blood flow to the kidney stimulates certain kidney cells to secrete the proteolytic enzyme renin, which converts the inactive angiotensinogen globulin in the blood into angiotensin I. Another enzyme then converts angiotensin I into angiotensin II, its active form. This peptide, in turn, stimulates the secretion of aldosterone by the adrenal cortex. Pathologically elevated aldosterone secretion with concomitant excessive retention of salt and water often results in edema.
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The steroid hormone found in the biologically active amorphous fraction that remains after separation of the various crystalline steroid substances, such as cortisol and corticosterone, from adrenal extracts. In solution, aldosterone exists as an equilibrium mixture of aldo and lactol forms (see illustration).

Structures for two forms of aldosterone in an equilibrium mixture, ( a ) aldo and ( b ) lactolenlarge picture
Structures for two forms of aldosterone in an equilibrium mixture, (a) aldo and (b) lactol

The chief function of aldosterone is the regulation of electrolyte metabolism, that is, promotion of sodium retention and enhancement of potassium excretion. Aldosterone is the most potent of the hormones which are concerned in this type of metabolism. See Adrenal gland, Hormone, Steroid

McGraw-Hill Concise Encyclopedia of Bioscience. © 2002 by The McGraw-Hill Companies, Inc.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.



(also electrocortin, or aldocortin), an adrenocortical hormone of the group of corticosteroids. It regulates mineral metabolism in the organism and is the basic mineralocorticoid. The molecular mass is 360.43.

Aldosterone was isolated in a crystalline form in 1953 and synthesized in 1959 by Wettstein. It helps to retain sodium ions (Na+) in the organism and to eliminate potassium ions (K+) in the urine, saliva, and perspiration. A deficiency of Na+ and an elevated K+ content in food lead to an increase in the formation of aldosterone. An insufficiency of aldosterone—for example, with adrenalectomy or with Addison’s disease—leading to an acute loss of Na, imperils the life of the organism. The increased formation of aldosterone—for example, with adrenal tumors and certain heart and kidney diseases—causes the retention of water in the organism (edema), an increase in blood pressure, and so forth. The level of aldosterone secretion is related to the relative Na+ and K+ content in the blood plasma and is regulated by the mesencephalon, which secretes the neurohormone adrenoglomerulotropine with the participation of angiotensin and renin, which is formed in the kidneys and the vegetative nervous system.


Berzin, T. Biokhimiia gormonov. Moscow, 1964. Page 259. (Translated from the German.)


The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.


C21H28O5 A steroid hormone extracted from the adrenal cortex that functions chiefly in regulating sodium and potassium metabolism.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
In 2006, Spence [13] suggested that physiologically individualised therapy based on phenotyping with plasma renin and aldosterone had the potential to eliminate or at least markedly diminish the racial disparities in hypertension and stroke in the USA.
"However, if your hypertension remains resistant, your doctor may further customize your drug regimen by switching you to a different diuretic if you've been taking hydrochlorothiazide, or prescribing spironolactone, a medication that reduces the effect of aldosterone," Dr.
Severe hyponatraemia, hyperkalaemia, hyperreninaemia and, paradoxially, significant high plasma aldosterone concentration are present in pseudohypoaldosteronism and urinary sodium loss is significant.
"Aldosterone is associated with glucose homeostasis and diabetes mellitus risk with graded associations among Chinese-Americans and blacks, suggesting that pleiotropic effects of aldosterone may represent a modifiable mechanism in diabetes mellitus pathogenesis with potential racial/ethnic variation," the authors write.
The plasma aldosterone level is normal or high, and plasma rennin activity (PRA) is low.
There are four suppression tests used to confirm the alterations: oral sodium load, oral fludrocortisone load, oral captopril load and saline infusion to suppress aldosterone secretion; with the first and last being the most commonly used (10).
[2] This results in increased mineralocorticoid like activity as there are structural similarities between cortisol and aldosterone, with increased Na+ and water retention in conjunction with increased H+ and K+ excretion.
In particular, plasma aldosterone was lower in patients with pituitary CS (P = 0.0040) and ectopic ACTH secretion (P = 0.0230) than in those in whom CS was excluded (Table 2).
Aldosterone is vital for controlling blood pressure and is created by the adrenal glands.
The steroid hormone aldosterone acts on a mineralocorticoid receptor in the renal collecting ducts through a protein kinase mechanism leading to stimulation of Na+ reabsorption and active secretion of both H+ and K with potential risk for hyperkalaemia and acidosis in case of aldosterone deficiency [4, 5].
The overactivation of RAAS results in the accumulation of aldosterone, which has been confirmed to aggravate myocardial oxidative stress and fibrosis [15].
Aldosterone, a hormone produced in the zona glomerulosa of the adrenal glands, has a major impact on metabolic pathways and is connected to multiple cardiovascular pathologies including endothelial dysfunction, thrombosis, and myocardial as well as vascular fibrosis [3].