Adrenal Glands Introduction.
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| Adrenal Gland . |
[1]. Adrenal glands are called the ‘life-saving glands’ or ‘essential endocrine glands’.
[2]. It is because the absence of adrenocortical hormones causes death within 3 to 15 days and absence of adreno-medullary hormones, drastically decreases the resistance to mental and physical stress.
Functional Anatomy of Adrenal Glands .
[1]. There are two adrenal glands. Each gland is situated on the upper pole of each kidney.
[2]. Because of the situation, adrenal glands are otherwise called suprarenal glands.
[3]. Each gland weighs about 4 g.
Parts of Adrenal Glands .
Adrenal gland is made of two distinct parts:
1. Adrenal cortex: Outer portion, constituting 80% of the gland .
2. Adrenal medulla: Central portion, constituting 20% of the gland.
[1]. These two parts are different from each other in development, structure and functions.
[2]. Adrenal medulla develops from the neural crest, which gives origin to sympathetic nervous system. So, its secretions and functions resemble that of sympathetic nervous system.
[3]. Adrenal cortex develops from the mesonephros, which give rise to the renal tissues.
[4]. It secretes entirely a different group of hormones known as corticosteroids.
Histology of Adrenal Cortex .
[1]. Adrenal cortex is formed by three layers of structure.
[2]. Each layer is distinct from one another.
1. Outer zona glomerulosa .
2. Middle zona fasciculata .
3. Inner zona reticularis .
Hormones of Adrenal Cortex .
[1]. Adrenocortical hormones are steroids in nature, hence the name ‘corticosteroids’.
[2]. Based on their functions, corticosteroids are classified into three groups:
1. Mineralocorticoids .
2. Glucocorticoids .
3. Sex hormones.
Synthesis ,Transport & Fate of Adrenocortical Hormones .
Synthesis of Hormone .
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| Synthesis of aldosterone . |
[1]. All adrenocortical hormones are steroid in nature and are synthesized mainly from cholesterol that is absorbed directly from the circulating blood.
[2]. Small quantity of cholesterol is also synthesized within the cortical cells from acetyl coenzyme A (acetyl-CoA).
Transport of Hormone .
Mineralocorticoids .
[1]. Mineralocorticoids are transported in blood by binding with plasma proteins, especially globulins.
[2]. The binding is loose and 50% of these hormones are present in free form.
Glucocorticoids .
[1]. Glucocorticoids are transported by a special plasma protein known as glucocorticoids-binding globulin or transcortin .
[2]. Ninety four percent of glucocorticoids are transported by this protein, whereas about 6% of them are found free in plasma.
[3]. Albumin plays a very little role in glucocorticoid transport.
Sex Hormones .
Adrenal sex hormones are transported by another special plasma protein known as sex hormone-binding globulin.
Fate of Corticosteroids .
[1]. Corticosteroids are degraded mainly in the liver and conjugated to form glucuronides and to a lesser extent, form sulfates.
[2]. About 25% of corticosteroids are excreted in bile and feces and remaining 75%, in the urine.
Mineralocorticoids .
[1]. Mineralocorticoids are the corticosteroids that act on the minerals (electrolytes), particularly sodium and potassium.
[2]. Mineralocorticoids are:
1. Aldosterone .
2. 11-deoxycorticosterone.
Source of Secretion of mineralocorticoids .
Mineralocorticoids are secreted by zona glomerulosa of adrenal cortex.
Chemistry & Half-life of mineralocorticoids .
[1]. Mineralocorticoids are C21 steroids having 21 carbon atoms.
[2]. Half-life of mineralocorticoids is 20 minutes.
Daily output and plasma level of mineralocorticoids .
Hormone Daily output
(µg) Plasma level
(µg/dL) .
(µg) Plasma level
(µg/dL) .
Aldosterone 0.15 0.006 .
11-Deoxycorticosterone 0.2 0.006 .
Functions of mineralocorticoids .
Ninety percent of mineralocorticoid activity is provided by aldosterone.
Life-saving Hormone .
[1]. Aldosterone is very essential for life and it maintains the osmolarity and volume of ECF.
[2]. It is usually called life-saving hormone because, its absence causes death within 3 days to 2 weeks. [3]. Aldosterone has three important functions.
[4]. It increases:
1. Reabsorption of sodium from renal tubules .
2. Excretion of potassium through renal tubules .
3. Secretion of hydrogen into renal tubules.
Actions of aldosterone are:
1. On Sodium Ions .
[1]. Aldosterone acts on the distal convoluted tubule and the collecting duct and increases the reabsorption of sodium.
[2]. During hypersecretion of aldosterone, the loss of sodium through urine is only few milligram per day.
[3]. But during hyposecretion of aldosterone, the loss of sodium through urine increases (hypernatriuria) up to about 20 g/day.
[4]. It proves the importance of aldosterone in regulation of sodium ion concentration and osmolality in the body.
2. On Extracellular Fluid Volume .
[1]. When sodium ions are reabsorbed from the renal tubules, simultaneously water is also reabsorbed. [2]. Water reabsorption is almost equal to sodium reabsorption; so the net result is the increase in ECF volume.
[3]. Even though aldosterone increases the sodium reabsorption from renal tubules, the concentration of sodium in the body does not increase very much because water is also reabsorbed simultaneously.
[4]. But still, there is a possibility for mild increase in concentration of sodium in blood (mild hypernatremia).
[5]. It induces thirst, leading to intake of water which again increases the ECF volume and blood volume.
3. On Blood Pressure .
Increase in ECF volume and the blood volume finally leads to increase in blood pressure.
Aldosterone escape or escape phenomenon .
Aldosterone escape refers to 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 .
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| Aldosterone escape . |
[1]. When aldosterone level increases, there is excess retention of sodium and water. This increases the volume of ECF and blood pressure.
[2]. Aldosterone-induced high blood pressure decreases the ECF volume through two types of reactions:
1. It stimulates secretion of atrial natriuretic peptide (ANP) from atrial muscles of the heart: ANP causes excretion of sodium in spite of increase in aldosterone secretion .
2. It causes pressure diuresis (excretion of excess salt and water by high blood pressure) through urine. This decreases the salt and water content in ECF, in spite of hypersecretion of aldosterone .
[3]. Besides ANP, two more natriuretic peptides called brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) are also secreted by cardiac muscle .
[4]. BNP and CNP also have similar actions of ANP on sodium excretion.
4. On Potassium Ions .
[1]. Aldosterone increases the potassium excretion through the renal tubules.
[2]. When aldosterone is deficient, the potassium ion concentration in ECF increases leading to hyperkalemia.
[3]. Hyperkalemia results in serious cardiac toxicity, with weak contractions of heart and development of arrhythmia.
[4]. In very severe conditions, it may cause cardiac death.
[5]. When aldosterone secretion increases, it leads to hypokalemia and muscular weakness.
5. On Hydrogen Ion Concentration .
[1]. While increasing the sodium reabsorption from renal tubules, aldosterone causes tubular secretion of hydrogen ions.
[2]. To some extent, secretion of hydrogen ions is in exchange for sodium ions. It obviously reduces the hydrogen ion concentration in the ECF.
[3]. In normal conditions, aldosterone is essential to maintain acid-base balance in the body.
[4]. In hypersecretion, it causes alkalosis and in hyposecretion, it causes acidosis.
6. On Sweat Glands and Salivary Glands .
[1]. Aldosterone has almost the similar effect on sweat glands and salivary glands as it shows on renal tubules.
[2]. Sodium is reabsorbed from sweat glands under the influence of aldosterone, thus the loss of sodium from the body is prevented. Same effect is shown on saliva also. Thus, aldosterone helps in the conservation of sodium in the body.
7. On Intestine .
[1]. Aldosterone increases sodium absorption from the intestine, especially from colon and prevents loss of sodium through feces.
[2]. Aldosterone deficiency leads to diarrhea, with loss of sodium and water.
Mode of Action of mineralocorticoids .
Aldosterone acts through the messenger RNA (mRNA) mechanism.
Sequence of Events .
[1] . Since aldosterone is lipid soluble, it diffuses readily into the cytoplasm of the tubular epithelial cells through the lipid layer of the cell membrane .
[2] . In the cytoplasm, aldosterone binds with the specific receptor protein .
[3] . Aldosterone-receptor complex diffuses into the nucleus where it binds to deoxyribonucleic acid (DNA) and causes formation of mRNA .
[4] . The mRNA diffuses back into the cytoplasm and causes protein synthesis along with ribosomes. Most of the synthesized proteins are in the form of enzymes. One of such enzymes is sodium-potassium ATPase, which helps in the transport of sodium and potassium.
Regulation of Secretion of mineralocorticoids .
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| Importance of aldosterone . |
[1]. Aldosterone secretion is regulated by four important factors which are given below in the order of their potency:
1. Increase in potassium ion (K+) concentration in ECF
2. Decrease in sodium ion (Na+) concentration in ECF
3. Decrease in ECF volume
4. Adrenocorticotropic hormone (ACTH).
[2]. Increase in the concentration of potassium ions is the most effective stimulant for aldosterone secretion. It acts directly on the zona glomerulosa and increases the secretion of aldosterone.
[3]. Decrease in sodium ion concentration and ECF volume stimulates aldosterone secretion through renin-angiotensin mechanism.
[4]. Renin secreted from juxtaglomerular apparatus of kidney acts on angiotensinogen in the plasma and converts it into angiotensin I, which is converted into angiotensin II by converting enzyme (ACE) secreted by lungs.
[5]. Angiotensin II acts on the zona glomerulosa to secrete more aldosterone. Aldosterone in turn, increases the retention of sodium and water and excretion of potassium. This leads to increase in the sodium ion concentration and ECF volume.
[6]. 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 .
[7]. Adrenocorticotropic hormone mainly stimulates the secretion of glucocorticoids. It has only a mild stimulating effect on aldosterone secretion.
Glucocorticoids .
[1]. Glucocorticoids act mainly on glucose metabolism.
[2]. Glucocorticoids are:
1. Cortisol .
2. Corticosterone .
3. Cortisone.
Source of Secretion of Glucocorticoids .
[1]. Glucocorticoids are secreted mainly by zona fasciculata of adrenal cortex.
[2]. A small quantity of glucocorticoids is also secreted by zona reticularis.
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| Synthesis of cortisol . |
Chemistry & Half-life of Glucocorticoids .
[1]. Glucocorticoids are C21 steroids having 21 carbon atoms.
[2]. Half-life of cortisol is 70 to 90 minutes and that of corticosterone is 50 minutes.
[3]. Half-life of cortisone is not known.
Daily output and plasma level of Glucocorticoids .
Hormone Daily output
(µg) Plasma level
(µg/dL)
(µg) Plasma level
(µg/dL)
Cortisol 10.0 13.9
Corticosterone 3.0 0.4 .
Functions of Glucocorticoids .
[1]. Cortisol or hydrocortisone is more potent and it has 95% of glucocorticoid activity.
[2]. Corticosterone is less potent showing only 4% of glucocorticoid activity.
[3]. Cortisone with 1% activity is secreted in minute quantity.
Life-protecting Hormone .
[1]. Like aldosterone, cortisol is also essential for life but in a different way.
[2]. Aldosterone is a life-saving hormone, whereas cortisol is a life-protecting hormone because, it helps to withstand the stress and trauma in life.
[3]. Glucocorticoids have metabolic effects on carbohydrates, proteins, fats and water. These hormones also show mild mineralocorticoid effect.
[4]. Removal of adrenal glands in human beings and animals causes disturbances of metabolism.
[5]. Exposure to even mild harmful stress after adrenalectomy, leads to collapse and death.
1. On Carbohydrate Metabolism .
[1]. Glucocorticoids increase the blood glucose level by two ways:
1. By promoting gluconeogenesis in liver from amino acids:
[1.1]. Glucocorticoids enhance the breakdown of proteins in extrahepatic cells, particularly the muscle. It is followed by release of amino acids into circulation.
[1.2]. From blood, amino acids enter the liver and get converted into glucose (gluconeogenesis)
2. By inhibiting the uptake and utilization of glucose by peripheral cells: This action is called antiinsulin action of glucocorticoids.
[2]. Hypersecretion of glucocorticoids increases the blood glucose level, resulting in hyperglycemia, glucosuria and adrenal diabetes.
[3]. Hyposecretion of these hormones causes hypoglycemia and fasting during adrenal insufficiency will be fatal. It decreases blood glucose level to a great extent, resulting in death.
2. On Protein Metabolism .
[1]. Glucocorticoids promote the catabolism of proteins, leading to:
1. Decrease in cellular proteins .
2. Increase in plasma level of amino acids .
3. Increase in protein content in liver.
[2]. Glucocorticoids cause catabolism of proteins by the following methods:
1. By releasing amino acids from body cells (except liver cells) into the blood
2. By increasing the uptake of amino acids by hepatic cells from blood. In hepatic cells, the amino acids are used for the synthesis of proteins and carbohydrates (gluconeogenesis).
[3]. Thus, glucocorticoids cause mobilization of proteins from tissues other than liver.
[4]. In hypersecretion of glucocorticoids, there is excess catabolism of proteins, resulting in muscular wasting and negative nitrogen balance.
3. On Fat Metabolism .
[1]. Glucocorticoids cause mobilization and redistribution of fats.
[2]. Actions on fats are:
1. Mobilization of fatty acids from adipose tissue .
2. Increasing the concentration of fatty acids in blood .
3. Increasing the utilization of fat for energy.
[3]. Glucocorticoids decrease the utilization of glucose.
[4]. At the same time, these hormones mobilize fats and make the fatty acids available for utilization, by which energy is liberated.
[5]. It leads to the formation of a large amount of ketone bodies. It is called ketogenic effect of glucocorticoids.
[6]. Hypersecretion of glucocorticoids causes an abnormal type of obesity by increasing the deposition of fat in certain areas such as abdomen, chest, face and buttocks.
4. On Water Metabolism .
[1]. Glucocorticoids play an important role in the maintenance of water balance, by accelerating excretion of water.
[2]. The adrenal insufficiency causes water retention and water intoxication after intake of large quantity of water.
5. On Mineral Metabolism .
[1]. Glucocorticoids enhance the retention of sodium and to lesser extent, increase the excretion of potassium.
[2]. Thus, hypersecretion of glucocorticoids causes edema, hypertension, hypokalemia and muscular weakness.
[3]. Glucocorticoids decrease the blood calcium by inhibiting its absorption from intestine and increasing the excretion through urine.
6. On Bone .
[1]. Glucocorticoids stimulate the bone resorption (osteoclastic activity) and inhibit bone formation and mineralization (osteoblastic activity).
[2]. So, in hypersecretion of glucocorticoids, osteoporosis occurs.
7. On Muscles .
Glucocorticoids increase the catabolism of proteins in muscle. So, hypersecretion causes muscular weakness due to loss of protein.
8. On Blood Cells .
[1]. Glucocorticoids decrease the number of circulating eosinophils by increasing the destruction of eosinophils in reticuloendothelial cells.
[2]. These hormones also decrease the number of basophils and lymphocytes and increase the number of circulating neutrophils, RBCs and platelets.
9. On Vascular Response .
[1]. Presence of glucocorticoids is essential for the constrictor action of adrenaline and noradrenaline .
[2]. In adrenal insufficiency, the blood vessels fail to respond to adrenaline and noradrenaline, leading to vascular collapse.
10. On Central Nervous System .
[1]. Glucocorticoids are essential for normal functioning of nervous system.
[2]. Insufficiency of these hormones causes personality changes like irritability and lack of concentration.
[3]. Sensitivity to olfactory and taste stimuli increases in adrenal insufficiency.
11. Permissive Action of Glucocorticoids .
[1]. Permissive action of glucocorticoids refers to execution of actions of some hormones only in the presence of glucocorticoids.
[2]. Examples are
1. Calorigenic effect of glucagon .
2. Lipolytic effect of catecholamines .
3. Vascular effects of catecholamines .
4. Bronchodilator effect of catecholamines.
12. On Resistance to Stress .
[1]. Exposure to any type of stress, either physical or mental, increases the secretion of adrenocorticotropic hormone (ACTH), which in turn increases glucocorticoid secretion.
[2]. The increase in glucocorticoid level is very essential for survival during stress conditions, as it offers high resistance to the body against stress.
[3]. Glucocorticoids enhance the resistance by the following ways:
1. Immediate release and transport of amino acids from tissues to liver cells for the synthesis of new proteins and other substances, which are essential to withstand the stress .
2. Release of fatty acids from cells for the production of more energy during stress .
3. Enhancement of vascular response to catecholamines and fatty acid-mobilizing action of catecholamines, which are necessary to withstand the stress .
4. Prevention of severity of other changes in the body caused by stress.
13. Anti-inflammatory Effects .
[1]. Inflammation is defined as a localized protective response induced by injury or destruction of tissues.
[2]. When the tissue is injured by mechanical or chemical factors, some substances are released from the affected area.
[3]. These substances produce series of reactions in the affected area:
1. Chemical substances such as histamine, serotonin, leukotrienes, prostaglandins and bradykinin, which are released from damaged tissue cause vasodilatation and erythema (rushing of blood) in the affected area .
2. From blood, many leukocytes, particularly neutrophils and monocytes infiltrate the affected area. Leukocytes play an important role in the defensive mechanism .
3. Vasodilator substances released in the affected area increase the permeability of capillary membrane, resulting in oozing out of fluid from blood into interstitial space .
4. Coagulation occurs in the interstitial fluid because of fibrinogen and other proteins, which are leaked out from blood
5. Finally, edema occurs in that area which may be non-pitting type because of hard clot formation.
[4]. Glucocorticoids prevent the inflammatory reactions. Even if inflammation has already started, the glucocorticoids cause an early resolution of inflammation and rapid healing.
[5]. Glucocorticoids prevent the inflammatory changes by:
1. Inhibiting the release of chemical substances from damaged tissues and thereby preventing vasodilatation and erythema in the affected area .
2. Causing vasoconstriction through the permissive action on catecholamines. This also prevents rushing of blood to the injured area .
3. Decreasing the permeability of capillaries and preventing loss of fluid from plasma into the affected tissue .
4. Inhibiting the migration of leukocytes into the affected area .
5. Suppressing T cells and other leukocytes, so that there is reduction in the reactions of tissues which enhance the inflammatory process.
14. Anti-allergic Actions .
Corticosteroids prevent various reactions in allergic conditions as in the case of inflammation.
15. Immunosuppressive Effects .
[1]. Glucocorticoids suppress the immune system of the body by decreasing the number of circulating T lymphocytes.
[2]. It is done by suppressing proliferation of T cells and the lymphoid tissues (lymph nodes and thymus).
[3]. Glucocorticoids also prevent the release of interleukin-2 by T cells. Thus, hypersecretion or excess use of glucocorticoids decreases the immune reactions against all foreign bodies entering the body.
[4]. It leads to severe infection causing death. Immunological reactions, which are common during organ transplantation, may cause rejection of the transplanted tissues.
[5]. Glucocorticoids are used to suppress the immunological reactions because of their immunosuppressive action.
Mode of Action of Glucocorticoids .
1. Glucocorticoids bind with receptors to form hormone receptor complex, which activates DNA to form mRNA.
2. mRNA causes synthesis of enzymes, which alter the cell function.
Regulation of Secretion of Glucocorticoids .
1. Anterior pituitary regulates glucocorticoid secretion by secreting adrenocorticotropic hormone (ACTH).
2. ACTH secretion is regulated by hypothalamus through corticotropin-releasing factor (CRF).
Role of Anterior Pituitary – ACTH .
Anterior pituitary controls the activities of adrenal cortex by secreting ACTH. ACTH is mainly concerned with the regulation of cortisol secretion and it plays only a minor role in the regulation of mineralocorticoid secretion.
Source of secretion of ACTH .
ACTH is secreted by the basophilic chromophilic cells of anterior pituitary.
Chemistry, plasma level and half-life of ACTH .
[1]. ACTH is a single chained polypeptide with 39 amino acids.
[2]. The daily output of this hormone is 10 ng and the concentration in plasma is 3 ng/dL.
[3]. Half-life of ACTH is 10 minutes.
Synthesis of ACTH .
[1]. ACTH is synthesized from a protein called preproopiomelanocortin (POMC). Along with ACTH, the POMC gives rise to some more byproducts called β-lipotropin, γ-lipotropin and β-endorphin.
[2]. Two more byproducts, namely α-melanocyte-stimulating hormone (α-MSH) and β-melanocyte-stimulating hormone (β-MSH) are also secreted in animals. However, MSH activity is shown by ACTH and other byproducts from POMC in human beings.
Actions of ACTH .
ACTH is necessary for the structural integrity and secretory activity of adrenal cortex. It has other functions also.
Actions of ACTH on adrenal cortex (Adrenal actions) .
1. Maintenance of structural integrity and vascularization of zona fasciculata and zona reticularis of adrenal cortex. In hypophysectomy, these two layers in the adrenal cortex are atrophied .
2. Conversion of cholesterol into pregnenolone, which is the precursor of glucocorticoids. Thus, adrenocorticotropic hormone is responsible for the synthesis of glucocorticoids .
3. Release of glucocorticoids .
4. Prolongation of glucocorticoid action on various cells.
Other (Nonadrenal) actions of ACTH .
1. Mobilization of fats from tissues .
2. Melanocyte-stimulating effect. Because of structural similarity with melanocyte-stimulating hormone (MSH), ACTH shows melanocyte-stimulating effect. It causes darkening of skin by acting on melanophores, which are the cutaneous pigment cells containing melanin.
Mode of action of ACTH .
ACTH acts by the formation of cyclic AMP.
Role of Hypothalamus .
[1]. Hypothalamus also plays an important role in the regulation of cortisol secretion by controlling the ACTH secretion through corticotropin-releasing factor (CRF). It is also called corticotropin-releasing hormone.
[2]. CRF reaches the anterior pituitary through the hypothalamohypophyseal portal vessels.
[3]. CRF stimulates the corticotropes of anterior pituitary and causes the synthesis and release of ACTH.
[4]. CRF secretion is induced by several factors such as emotion, stress, trauma and circadian rhythm. CRF in turn, causes release of ACTH, which induces glucocorticoid secretion.
Feedback Control .
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| Regulation of cortisol secretion . |
Cortisol regulates its own secretion through negative feedback control by inhibiting the release of CRF from hypothalamus and ACTH from anterior pituitary .
Circadian rhythm of ACTH .
[1]. ACTH secretion follows circadian rhythm , i.e. it varies in different periods of the day.
[2]. The rate of secretion of both ACTH and CRF is high in the morning and low in the evening.
[3]. Hypothalamus plays an important role in the circadian fluctuations of ACTH secretion.
Adrenal Sex hormones
[1]. Adrenal sex hormones are secreted mainly by zona reticularis.
[2]. Zona fasciculata secretes small quantities of sex hormones.
[3]. Adrenal cortex secretes mainly the male sex hormones, which are called androgens. But small quantity of estrogen and progesterone are also secreted by adrenal cortex.
Synthesis of sex hormones .
[1]. Androgens secreted by adrenal cortex:
1. Dehydroepiandrosterone
2. Androstenedione
3. Testosterone.
[4]. Dehydroepiandrosterone is the most active adrenal androgen. Androgens, in general, are responsible for masculine features of the body .
[5]. But in normal conditions, the adrenal androgens have insignificant physiological effects, because of the low amount of secretion both in males and females.
[6]. In congenital hyperplasia of adrenal cortex or tumor of zona reticularis, an excess quantity of androgens is secreted.
[7]. In males, it does not produce any special effect because, large quantity of androgens are produced by testes also. But in females, the androgens produce masculine features.
[8]. Some of the androgens are converted into testosterone.
[9]. Testosterone is responsible for the androgenic activity in adrenogenital syndrome or congenital adrenal hyperplasia.
Exogenous Steroids .
[1]. Corticosteroids are used as drugs since long. Exogenous steroids are extracted from adrenal cortex of animals or prepared artificially.
[2]. Commercially available synthetic drugs with corticosteroid effects are widely used.
[3]. These drugs are either used as replacement of natural hormones (replacement therapy) in patients with deficiency disorders such as Addison disease or to treat a variety of other conditions such as arthritis, allergic conditions, asthma, skin disorders, etc.
Synthetic Steroids .
Synthetic steroids that are commonly used are:
1. Cortisone and hydrocortisone, which are used for replacement therapy have both glucocorticoid and mineralocorticoid effects
2. Prednisolone has more glucocorticoid activity than mineralocorticoid activity
3. Fludrocortisone (9-fluorocortisol) has more mineralocorticoid activity than glucocorticoid activity. It has most potent mineralocorticoid effect.
4. Dexamethasone has only glucocorticoid effect.
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