Mineralocorticoids
Mineralocorticoids are corticosteroids that act on minerals (electrolytes), particularly sodium and potassium. Mineralocorticoids are:
- Aldosterone
- 11-Deoxycorticosterone.
Mineralocorticoids Source Of Secretion: The mineralocorticoids are secreted by zona glomerulosa of adrenal cortex.
Mineralocorticoids Chemistry And Half-Life: Mineralocorticoids are C21 steroids having 21 carbon atoms. The half-life of mineralocorticoids is 20 minutes.
Mineralocorticoids Daily Output And Plasma Level: The daily output and plasma level of mineralocorticoids are given in Table.
Read And Learn More: Medical Physiology Notes
Functions Of Mineralocorticoids: Ninety percent of mineralocorticoid activity is provided by aldosterone.


Aldosterone Life-Saving Hormone
- Aldosterone is very essential for life and it is usually called life saving hormone. Total loss of corticosteroids usually causes death within 3 days to 2 weeks. It is mainly because of loss of mineralocorticoids.
- During mineralocorticoid deficiency, the potassium ion concentration of the ECF rises markedly. The concentration of sodium and chloride ions decreases. The total ECF volume and blood volume are also greatly reduced. All these changes lead to cardiac dysfunction, a shock-like state, and finally death. The entire sequence can be prevented and life can be saved by the administration of aldosterone. That is why, it is known as life-saving hormone.
- Three important functions of aldosterone are:
- It increases the reabsorption of sodium from renal tubules
- It increases the excretion of potassium through renal tubules
- It increases secretion of hydrogen ions into the tubules
- The actions of aldosterone are:
- On Sodium Ions:
- Aldosterone acts on the distal convoluted tubule and the collecting duct and increases the reabsorption of sodium. During hypersecretion of aldosterone, the loss of sodium through urine is only few milligrams per day.
- But during the hyposecretion of aldosterone, the loss of sodium through urine increases (hypernatriuria) up to about 20 g/day. It proves the importance of aldosterone in regulation of sodium ion concentration and osmolality in the body.
- On Extracellular Fluid Volume
- When sodium ions are reabsorbed from the renal tubules, simultaneously water is also reabsorbed. Water reabsorption is almost equal to sodium reabsorption so the net result is the increase in ECF volume.
- Even though aldosterone increases the sodium reabsorption from the renal tubules, the concentration of sodium in the body does not increase to that extent because of simultaneous water reabsorption.
- But still, there is a possibility for a mild increase in the concentration of sodium in the blood (mild hypernatremia). It induces thirst leading to intake of water which again increases the ECF volume and blood volume.
- On Blood Pressure: Increase in ECF volume and blood volume finally leads to increase in blood pressure.
- Aldosterone escape or escape phenomenon: Aldosterone escape refers to the escape of the kidney from salt-retaining effects of excess administration or secretion of aldosterone as in the case of primary hyperaldosteronism.
- Mechanism of aldosterone escape: When the aldosterone level increases, there is excess retention of sodium and water. This increases the volume of ECF and blood pressure. Aldosterone-induced high blood pressure decreases the ECF volume through two types of reactions:
- It stimulates secretion of atrial natriuretic peptide (ANP) from the atrial muscles of the heart: ANP causes excretion of sodium in spite of the increase in aldosterone secretion
- It causes pressure dieresis (excretion of excess salt and water by high blood pressure) through urine. This decreases the salt and water content in ECF in spite of the hypersecretion of aldosterone.
- Because of aldosterone escape, edema does not occur in primary hyperaldosteronism. Besides ANP, two more natriuretic peptides called brain natriuretic peptide and C-type natriuretic peptide (CNP) are also secreted by cardiac muscle. BNP and CNP also have similar actions of ANP on sodium excretion.
- The escape phenomenon does not occur in some of the conditions such as heart failure, cirrhosis of the liver, and nephritic syndrome. In these conditions, the increased aldosterone increases sodium and water retention faulting in increased ECF volume and edema.
- Significance of aldosterone escape: When aldosterone secretion is decreased or absent, a very large amount of salt is lost in the urine. It decreases the content of salt and water in ECF resulting in severe dehydration and low blood volume. Low blood volume leads to circulatory shock. If treatment is not given immediately, dehydration leads to death within few days.
- On Potassium Ions: Aldosterone increases the potassium excretion through the renal tubules. When aldosterone is deficient, the potassium ion concentration in ECF increases leading to hyperkalemia. Flyperkalemia results in serious cardiac toxicity with weak contractions of heart and development of arrhythmia. In very severe conditions, it may cause cardiac death. When aldosterone secretion increases, it leads to hypokalemia and muscular weakness.
- On Hydrogen Ion Concentration: While increasing the sodium reabsorption from the renal tubules, aldosterone causes tubular secretion of hydrogen ions. To some extend, secretion of hydrogen ions is in exchange for sodium ions. It obviously reduces the hydrogen ion concentration in the ECF. In normal conditions, aldosterone is essential to maintain acid- base balance in the body. In hypersecretion, it causes alkalosis and in hyposecretion, it causes acidosis.
- On Sweat Glands and Salivary Glands: Aldosterone has almost the similar effect on sweat ^ glands and salivary glands as it shows on renal tubules. Sodium is reabsorbed from sweat glands under the influence of aldosterone, thus the loss of sodium from the body is prevented. It becomes more important in hot environment when lot of sweat is excreted. Same effect is shown on saliva also. Thus, aldosterone helps conservation of sodium in the body.
- On Intestine: Aldosterone greatly enhances sodium absorption from the intestine, especially in the colon, and prevents loss of sodium through feces. Aldosterone deficiency leads to the loss of sodium and water through the feces resulting in diarrhea.
- On Sodium Ions:
- Three important functions of aldosterone are:

Aldosterone Mode Of Action: Aldosterone acts through the messenger RNA mechanism.

The sequence of events:
-
- Since aldosterone is lipid soluble, it diffuses readily into the cytoplasm of the tubular epithelial cells through the lipid layer of the cell membrane
- In the cytoplasm, aldosterone binds with the specific receptor protein
- The aldosterone-receptor complex diffuses into the nucleus. Here, it undergoes further alterations including binding to DNA and formation of mRNA
- The mRNA diffuses back into the cytoplasm. In the cytoplasm, along with ribosomes, it causes protein synthesis. Most of the synthesized proteins are in the form of enzymes. One of such enzyme which help in the transport of sodium and potassium through the sodium-potassium pump is the sodium-potassium ATPase.
Aldosterone Regulation Of Secretion: Aldosterone secretion is regulated by four important factors. The stimulatory agents for aldosterone secretion are given below in the order of their potency:
- Increase in potassium ion concentration in ECF
- Decrease in sodium ion concentration in ECF
- Decrease in ECF volume
- Adrenoccrticotropic hormone.

- An increase in the concentration of potassium ions is the most effective stimulant for aldosterone secretion. It acts directly on the zona glomerulus and increases the secretion of aldosterone.
- Decrease in sodium ion concentration and ECF volume stimulates aldosterone secretion through renin-angiotensin mechanism. Renin secreted from the juxtaglomerular apparatus of kidney acts on angiotensinogen in the plasma and converts it into angiotensin I, which is converted into angiotensin 2 by converting enzyme (ACE) secreted by lungs.
- Angiotensin 2 acts on the zona giomerulosa to secrete more aldosterone. Aldosterone in turn, increases the retention of sodium and water and excretion of potassium. This causes an increase in the sodium ion concentration and volume of ECF.
- Now, the increased sodium ion concentration and the ECF volume inhibit the juxtaglomerular apparatus and stop the release of renin. So, angiotensin II is not formed and release of aldosterone from adrenal cortex is stopped.
- Adrenocorticotropic hormone mainly stimulates the secretion of glucocorticoids. It has only a mild stimulating effect on aldosterone secretion.
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