| Mineralocorticoid | |
|---|---|
| Drug class | |
 Aldosterone, the majorendogenous mineralocorticoid | |
| Class identifiers | |
| Synonyms | Corticosteroid; Mineralocorticosteroid |
| ATC code | H02AA |
| Biological target | Mineralocorticoid receptor |
| Chemical class | Steroids |
| Legal status | |
| In Wikidata | |
Mineralocorticoids are a class ofcorticosteroids, which in turn are a class ofsteroid hormones. Mineralocorticoids are produced in theadrenal cortex and influence salt and water balances (electrolyte balance andfluid balance). The primary mineralocorticoid isaldosterone.
The name mineralocorticoid derives from early observations that these hormones were involved in the retention ofsodium, amineral. The primaryendogenous mineralocorticoid isaldosterone, although a number of other endogenous hormones (includingprogesterone[1] anddeoxycorticosterone) have mineralocorticoid function.
Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption ofwater, as well as the active secretion ofpotassium in the principal cells of the corticalcollecting tubule and active secretion ofprotons via protonATPases in the lumenal membrane of theintercalated cells of thecollecting tubule. This in turn results in an increase ofblood pressure andblood volume.
Aldosterone is produced in the zona glomerulosa of the cortex of theadrenal gland and its secretion is mediated principally byangiotensin II but also byadrenocorticotrophic hormone (ACTH) and localpotassium levels.
The effects of mineralocorticoids are mediated by slow genomic mechanisms throughnuclear receptors as well as by fast nongenomic mechanisms through membrane-associated receptors andsignaling cascades.
Mineralocorticoids bind to themineralocorticoid receptor in the cellcytosol, and are able to freely cross thelipid bilayer of the cell. This type ofreceptor becomes activated uponligand binding. After a hormone binds to the corresponding receptor, the newly formedreceptor-ligand complex translocates into thecell nucleus, where it binds to manyhormone response elements (HREs) in thepromoter region of the targetgenes in theDNA.
The opposite mechanism is calledtransrepression. Thehormone receptor without ligand binding interacts withheat shock proteins and prevents thetranscription of targeted genes.
Aldosterone andcortisol (aglucosteroid) have similar affinity for the mineralocorticoid receptor; however, glucocorticoids circulate at roughly 100 times the level of mineralocorticoids. An enzyme exists in mineralocorticoid target tissues to prevent overstimulation by glucocorticoids. This enzyme,11-beta hydroxysteroid dehydrogenase type II (Protein:HSD11B2), catalyzes the deactivation of glucocorticoids to 11-dehydro metabolites.Licorice is known to be an inhibitor of this enzyme and chronic consumption can result in a condition known aspseudohyperaldosteronism.[3]
Hyperaldosteronism (the syndrome caused by elevated aldosterone) is commonly caused by either idiopathic adrenal hyperplasia or by anadrenal adenoma. The two main resulting problems:
Hypoaldosteronism (the syndrome caused by underproduction of aldosterone) leads to the salt-wasting state associated withAddison's disease, although classicalcongenital adrenal hyperplasia and other disease states may also cause this situation. Acute underproduction (hemorrhagic adrenalitis) is often life-threatening.
An example of a synthetic mineralocorticoid isfludrocortisone (Florinef).
Importantantimineralocorticoids arespironolactone andeplerenone.
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