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Additional recommended knowledge
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 and deoxycorticosterone) have mineralocorticoid function.
Aldosterone acts on the kidneys to provide active reabsorption of sodium and an associated passive reabsorption of water, as well as the active secretion of potassium in the principle cells of the cortical collecting tubule and active secretion of protons via proton ATPases in the lumenal membrane of the intercalated cells of the collecting tubule. This in turn results in an increase of blood pressure and blood volume.
Mode of Action
Mineralocorticoids bind to the cytosolic mineralocorticoid receptor. This type of receptor gets activated upon ligand binding. After a hormone binds to the corresponding receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many hormone response elements (HRE) in the promoter region of the target genes in the DNA.
Aldosterone and cortisol 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 as pseudohyperaldosteronism.
18 hydroxy 11 deoxycorticosterone (also designated 18OH-DOC) is a steroid hormone probably used to conserve sodium and stimulate hydrogen ion (or acid) excretion. 18OH-DOC lowers urine pH but has no affect on potassium excretion. This would seem to indicate that 18OH-DOC's primary purpose is to stimulate hydrogen ion or ammonium excretion. Under low sodium intake 18 OH DOC is increased in serum. There is a marked increase in serum 18OH DOC after injection of insulin   and this may be due to the hypokalemic (low serum potassium) tendency after a rise in insulin  which in turn would make the serum more acidic. Since 18OH-DOC lowers urine pH (increases acidity) but has no affect on potassium excretion, this would seem to indicate that 18OH-DOC's primary purpose is to stimulate hydrogen ion or ammonium excretion. Its use by the body to conserve potassium would be indirect by virtue of hydrogen ion's interference with potassium excretion. This interference is further indicated because injecting sodium bicarbonate or even hyperventilating (breathing rapidly beyond need) can triple potassium excretion. The daily rhythm for potassium and hydrogen ion excretion show a rather close inverse relationship, which gives additional circumstantial support to the supposition that they compete at a common site. 18OH-DOC is strongly dependent on the potassium cell or plasma content, because in potassium deficient rats markedly less 18OH-DOC is converted to 18OH-corticosterone and less yet if sodium is deficient.
ACTH (a peptide hormone) has a large affect on 18OH DOC, causing 18OH DOC to go down to zero when ACTH does. This could be for the primary purpose of keeping serum immune enzymes and cell fluids at a high pH (alkaline) during internal infection, but not doing so during the intestinal infection of diarrhea, during which disease the resulting dehydration forces ACTH to decline. It probably is important normally to keep the vacuoles where pathogens are digested at a high pH because if the pH or alkalinity is not high enough, the pathogens inside the immune cells are not digested  and thus released intact. So when an intestinal disease is not calling for ACTH to decline, the indirect potassium conserving attribute of 18OH-DOC by virtue of stimulating acid excretion would be valuable, as would also increased acid excretion during internal disease be valuable.
18OH DOC may act primarily by blocking aldosterone's effect on potassium, and must have aldosterone to assist it with sodium. Nichols, et al, have been able to show that injection of 18OH-DOC, which raised blood levels of this hormone ten times, were more retentive of sodium than a similar amount of aldosterone. So there must be a synergism involved. At the same time, the ratio of sodium to potassium excretion declined very little for 18OH-DOC, while for aldosterone, the ratio fell to as little as 1/3 that of control men. This implies a considerable sparing of potassium by 18OH-DOC. Urine potassium excretion is not altered by 18OH-DOC injection.
Angiotensin II has very little effect on 18OH-DOC and is ambiguous nor does serum potassium above 4.8 mEq/litter (187 mg). This last is not surprising since 18OH-DOC should not be used by the body at high serum potassium. Under low sodium intake, 18OH-DOC rises in the serum. ACTH causes a marked increase in 18OH-DOC, probably by a generalized affect on the zona fasciculata of the adrenal cortex where 18OH-DOC is synthesized. So when it is necessary for sodium to be unloaded during the dehydration induced decline of ACTH  during diarrhea in order to preserve osmotic pressure, the resulting 18OH-DOC decline would assist in this.
Hyperaldosteronism (the syndrome caused by elevated aldosterone) generally results from adrenal neoplasms. The two main resulting problems:
Underproduction, or hypoaldosteronism, leads to the salt-wasting state associated with Addison's disease, although classical congenital adrenal hyperplasia and other disease states may also cause this situation.
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Mineralocorticoid". A list of authors is available in Wikipedia.|