Endocrine physiology of the adrenal gland

2021-06-17 03:32 PM

In the function of the adrenal medulla, which is related to sympathetic activity, sympathetic stimulation also induces secretion of adrenal medullary hormones.

Anatomical and organizational features

The adrenal gland consists of two small glands that sit on top of the kidneys, each weighing about 4g.

The adrenal gland consists of two distinct parts: the cortex (80%) and the medulla (20%).

Adrenal cortex

Consists of 3 separate layers (Fig.

The globular layer consists of very thin cells located on the outermost part of the gland, which produces the water-salt metabolism hormone mineralocorticoid (aldosterone).

The middle bundle layer produces glucocorticoids (cortisol).

The inner reticulum secretes androgens.

The bridge layer and the other two layers are affected by completely different factors. Factors that increase glomerulus proliferation and aldosterone secretion have no effect on the other two layers, and conversely, factors that increase cortisol and androgen secretion have no effect on the glomerulus.

Figure: Adrenal cortex.

Adrenal medulla

Located in the centre of the gland, it produces and secretes catecholamines, considered two large sympathetic ganglia from which neurons lose their axons and become secretory cells.

The adrenal medullary function is related to sympathetic activity, sympathetic stimulation also induces secretion of adrenal medullary hormones, and these hormones have effects like those of the sympathetic nervous system.

The adrenal gland is small but vital.

In experimental animals, if two adrenal modules are removed, the animal will have blood pressure disorders but after a period of time it will return to normal, whereas if two parts of the cortex are removed, the animal will die in a few days to a few weeks because electrolyte disturbances and stress.

Adrenal cortex hormones

Adrenal cortex hormones are derived from cholesterol forming steroids. Cholesterol goes through stages, forming 3 types:

Glucocorticoid (Gc) : Cortisol, corticosterone.

Mineralocorticoid (Gm) : Aldosterone, 11-desoxycorticosterone.

Sex hormones: Androgen, oestrogen (stain).

About 30 different steroids have been isolated from the adrenal cortex, but only two have an important function, cortisol, and aldosterone. All adrenocortical hormones are synthesized from acetate samples by the cholesterol pathway (diagram).

Schematic diagram: Biosynthesis of the adrenocortical hormone.

In the blood 94% of cortisol is in a conjugated form, mainly bound to a globulin, called transporting. 50% of aldosterone is loosely bound to plasma proteins.

In the target tissue, cortisol acts and is destroyed within 1-2 hours and aldosterone in about 30 minutes. Adrenal cortex hormones are destroyed in the liver, 25% excreted by the biliary tract and 75% by the renal route.

Normal cortisol concentration is about 12 (g/dl, excretion 15-20 mg/day, aldosterone concentration is about 6 ng/dl, excretion 150-250 (g/day).

Glucocorticoid group (Gc)

95% is due to the action of cortisol (hydrocortisone*)


Effects on metabolism:

Glucid: increase new sugar in the liver; decreased use of glucose in cells; increases blood glucose, can cause diabetes, like pituitary diabetes.

Protein: increased protein degradation in most body cells, except liver cells. Increase amino acid transfer into liver cells, increase protein synthesis in the liver, increase conversion of amino acids into glucose. Increases amino acid concentration, reduces amino acid transport into cells except for the liver.

Lipids: increased lipid degradation in adipose tissue causes increased plasma free fatty acid concentrations and increased utilization for energy; increased fatty acid oxidation in tissues.

Anti-stress effects:

When stressed, the body immediately increases the amount of ACTH, after a few minutes, a large amount of cortisol is secreted by the adrenal cortex, which can increase to 300mg/24 hours.

Probably because cortisol quickly mobilizes amino acids and stored fat, providing energy for the organization; At the same time, these amino acids are used to synthesize substances necessary for cell survival such as purines, pyrimidines, and creatine phosphate.

Anti-inflammatory effects:

Cortísol reduces all stages of the inflammatory process, especially at high doses, this effect is used clinically.

Because cortisol stabilizes lysosomal membranes in cells and inhibits phospholipase A2, prevents the formation of inflammatory substances such as leukotrienes, prostaglandins, which are two substances that cause vasodilation, increase temperature, increase capillary permeability in reactions. inflammatory response.

Anti-allergic effect:

Cortisol inhibits the release of histamine during antigen-antibody reactions, thereby reducing allergic phenomena.

Effects on blood cells:

Reduces the number of eosinophils, lymphocytes, and the size of lymph nodes and thymus.

Effects on the immune system:

Antibodies decrease, so long-term use of cortisol is susceptible to infection but is used to prevent graft rejection.

Effects on other endocrine glands:

Elevated levels of cortisol will reduce the conversion of T4 to T3 and increase the conversion of T3 to T4, reducing sex hormone levels.

Other effects:

Increased secretion of gastric juice, if prolonged use of cortisol can cause stomach ulcers, for the skeletal system, can inhibit bone formation, reduce cell proliferation, reduce protein synthesis deposition of bone.

Regulate secretions:

Cortisol is regulated by the ACTH of the yen by a counterregulatory mechanism. The rhythm of cortisol secretion corresponds to the rhythm of ACTH secretion.

Mineralocorticoid group (Gm) Aldosterone is the main hormone of this group


Increased reabsorption of Na ions and increased excretion of K and Cl ions in the renal tubules, leading to water reabsorption (mainly ADH-mediated), causing an increase in extracellular volume.

Elevated concentrations of aldosterone can increase the extracellular fluid volume by 5-15% and lead to an increase in arterial blood pressure by 15-25%.

In contrast, a decrease in aldosterone causes sodium loss, a decrease in extracellular fluid volume, and an increase in K+ ions that can cause myocardial toxicity.

The same effect as above occurs in the salivary and sweat glands.

This effect is especially important when the body is operating in a hot environment, thanks to aldosterone, the loss of salt through the skin through sweat will be reduced.

Regulate secretions:

Related to sodium metabolism, when blood sodium is high, blood aldosterone will decrease, sodium is excreted, and vice versa.

High concentrations of K+ in the extracellular fluid increase aldosterone secretion.

In addition, regulation is also through the Renin-angiotensin-aldosterone system

Sex hormone group

The sexual activity of adrenocortical androgens is minimal, evident in the presence of pathologically increased secretion.

Adrenal medullary hormones

Figure: Sympathetic nerves innervate the adrenal medulla with only preganglionic fibers, catecholamines are released into the bloodstream as hormones.

The adrenal medulla is a giant sympathetic ganglion that secretes catecholamines, which respond to nerve impulses along the sympathetic preganglionic fibres to the adrenal medulla, causing increased sympathetic nervous system activity (Fig.

Epinephrine, norepinephrine, and dopamine are called catecholamines. Normally, blood is 80% epinephrine and 20% norepinephrine.


The effects of epinephrine, norepinephrine is like those of the sympathetic nervous system, but the duration of action is longer. The most obvious effects of catecholamines are effects on cardiovascular and blood pressure.

There are norepinephrine and epinephrine receptors in all organs of the body. These receptors are divided into 2 types (and (; (receptor subdivided into (1 and (2 ), and ( then yes (1 and 2. Epinephrine binds both ( and , norepinephrine binds mainly to ). The effect of these two hormones on target cells depends on the type of receptor present in the target tissue.

Epinephrine makes the heartbeat faster, increases the force of contraction; On blood vessels, it causes vasoconstriction under the skin, dilation of coronary, cerebral and muscle vessels, causing a slight increase in blood pressure, a slight decrease in minimum blood pressure.

Norepinephrine has a similar effect to epinephrine but is stronger on blood vessels, increases the maximum and minimum blood pressure due to systemic vasoconstriction, other effects are weaker.

Catecholamines increase body metabolism, increase oxygen consumption and increase thermogenesis; Increases the breakdown of glycogen to glucose, thereby increasing blood glucose.

Regulate secretions

Most of the physiological effects on adrenal medullary hormone secretion are via the nervous system. Under baseline conditions, catecholamine excretion is low. Increased secretion is part of sympathetic activity in conditions such as stress, hypoglycaemia, cold, hypotension...

In normal subjects, the adrenal medulla secretes 0.2 (g/kg/min) epinephrine and 0.05 (g/kg/min) norepinephrine, thus maintaining normal blood pressure under total severance. Sympathetic nervous system Epinephrine concentrations are 170-520 pmol/l and norepinephrine 0.3-28 nmol/l in 18-22-year-old Vietnamese.

Adrenal dysfunctions

Adrenal cortex dysfunction

Acute (acute adrenal insufficiency): seen in sepsis, abrupt cessation of corticosteroids in long-term therapy.

Chronic (Addison's disease: black skin disease): due to autoimmune disease or due to adrenal tuberculosis or tumour compression. Manifestations of decreased secretion of cortisol, aldosterone, and mucosal pigmentation disorders.

Adrenal cortex advantage

Cushing's syndrome: Gc excess, adrenocortical tumour, or pituitary ACTH-secreting cell tumour. Fat patient, round face, thin limbs, red stretch marks in the abdomen, fat distribution disorder. Blood sugar increases, salt and water metabolism disorders, Na + stagnation, loss of K +, making the body week but blood pressure increases.

This syndrome may be caused by abuse of Gc in treatment.

Treatment is surgical removal and hormone replacement.

Conn's syndrome: adrenal glomerular, also known as primary hyperaldosteronism syndrome, manifests K+ loss, hypertension, gradually leading to hypokalaemia nephropathy with polyuria, muscle weakness, and metabolic alkalosis. chemical.

Adrenogenital syndrome

In boys, rapid growth, early puberty; In women, virilization, genital atrophy, amenorrhea. It is caused by a deficiency of 21-(-Hydroxylase, which deviates from synthesis, or by increased androgen production by the tumour.

Adrenal medullary hyperplasia

Pheochromocytoma, caused by pheochromocytoma of the adrenal medulla, secretes a lot of catecholamines, causing intermittent hypertension. Although it is a benign tumour, without surgery, the patient can die from hypertension and heart failure.