Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland.[4][5] It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon.[6] It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+) and potassium (K+) levels. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron.[6] 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.[7] When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease.[8] Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart.[7]


Skeletal formula of the fictitious aldehyde form[1]

Ball-and-stick model of the 18-acetal-20-hemiketal form based on crystallography[2][3]
Preferred IUPAC name
Other names
Aldocorten; Aldocortin; Electrocortin; Reichstein X; 18-Aldocorticosterone; 18-Oxocorticosterone; 11β,21-Dihydroxy-3,20-dioxopregn-4-en-18-al
3D model (JSmol)
ECHA InfoCard 100.000.128
MeSH Aldosterone
  • InChI=1S/C21H28O5/c1-20-7-6-13(24)8-12(20)2-3-14-15-4-5-16(18(26)10-22)21(15,11-23)9-17(25)19(14)20/h8,11,14-17,19,22,25H,2-7,9-10H2,1H3/t14-,15-,16+,17-,19+,20-,21+/m0/s1 Y
  • InChI=1/C21H28O5/c1-20-7-6-13(24)8-12(20)2-3-14-15-4-5-16(18(26)10-22)21(15,11-23)9-17(25)19(14)20/h8,11,14-17,19,22,25H,2-7,9-10H2,1H3/t14-,15-,16+,17-,19+,20-,21+/m0/s1
Molar mass 360.450 g·mol−1
H02AA01 (WHO)
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N verify (what is YN ?)

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 aldosterone secretion. The net effect of these drugs is to reduce sodium and water retention but increase retention of potassium. In other words, these drugs stimulate the excretion of sodium and water in urine, while they block the excretion of potassium.

Another example is spironolactone, a potassium-sparing diuretic of the steroidal spirolactone group, which interferes with the aldosterone receptor (among others) leading to lower blood pressure by the mechanism described above.

Aldosterone was first isolated by Sylvia Tait (Simpson) and Jim Tait in 1953; in collaboration with Tadeusz Reichstein.[10][11][12]

Share this article:

This article uses material from the Wikipedia article Aldosterone, and is written by contributors. Text is available under a CC BY-SA 4.0 International License; additional terms may apply. Images, videos and audio are available under their respective licenses.