Mode of action
Cortisone penetrates the cell wall of a body cell and binds to a suitable cortisone receptor inside the cell. These glucocorticoid receptors are found almost everywhere in the body, but they are found in greater numbers in the muscles, fatty tissue, skin, liver and lymphatic tissue. This active substance-receptor complex migrates into the cell nucleus, where the genetic material (DNA) is located.
The cortisone complex now attaches itself to certain sections of the genetic material via the receptor, which influences the formation of many different proteins. Among other things, these proteins play an important role in the development of inflammation or in the immune system. Due to this mechanism of inhibition of the production of proteins, after a certain time the desired and also the undesired effects of cortisone occur.
Since cortisone first inhibits the formation of the inflammatory and immune messenger substances, the effect only sets in after at least 20 minutes up to several days. However, other mechanisms of action of cortisone are also assumed, since effects are also observed that occur immediately. Cortisone also appears to act directly on the cell walls and to have a stabilizing effect on them.
This prevents water from leaking into the tissue, which is important, for example, if the throat swells due to allergic reactions or an insect bite caused by the fluid in the tissue and the respiratory tract may be at risk. In these cases, cortisone can be used as an emergency medication, but the exact mechanisms of this rapid cortisone action have not yet been sufficiently researched. Another effect of cortisone is used in the treatment of bronchial asthma.
Cortisone causes the mucous membranes to swell, thus dilating the airways that are narrowed by the asthma. In addition, cortisone reduces toughness and inhibits the formation of bronchial mucus and helps relax the cramped bronchial muscles. Among other things, glucocorticoids also have an influence on the electolytic balance (mineral corticoid effect).
This effect is more pronounced with the body’s own cortisone than with synthetic cortisone. Cortisone reduces fluid excretion and thus saves body salt, which leads to an increase in blood pressure. Potassium is an important body salt whose concentration in the blood must not be exceeded or fallen below. As a rule, treatment with cortisone does not require any additional potassium intake, but regular blood potassium checks are recommended.
Cortisone as a stress hormone
The cortisone concentration in the blood follows a natural daily rhythm (circadian rhythm) and therefore varies at different times during the day and at night. On average, the cortisone concentration in the blood increases around three o’clock in the morning. The growth hormone HGH (Human Growth Hormone), which is involved in the nightly recovery processes, is displaced by cortisone.
The formation of cortisone is controlled by the so-called internal clock. The cortisone prepares the body for waking up in the early morning. Between five and eight o’clock in the morning, the cortisone level reaches its highest values, after which it drops again continuously.
Elevated cortisone levels can be measured during stress, hypoglycemia or even during pregnancy. Cortisone protects the body from the negative consequences of severe stress and adapts it to current environmental conditions. For example, it raises the blood sugar level, thereby providing energy, and is involved in the contraction of blood vessels in the body, thus having a blood pressure-increasing effect.
The increased concentration of cortisone in the blood stimulates the body to sweat and slows down digestion (as more blood is directed to the muscles). Cortisone as a so-called “stress hormone” can also have effects on the central nervous system, where it can have a euphoric (triggering feelings of happiness) or dysphoric (bad-tempered, irritable, mood-altering) effect through stimulation. Cortisone belongs to the group of glucocorticoids.
These substances help the body so that it has sufficient nutrients and building substances available in stressful situations (but also in hunger phases between meals). Cortisone influences the so-called catabolic metabolism, which means that it mobilises the resources stored in the body. For example, cortisone promotes the production of blood sugar in the liver (gluconeogenesis) and stimulates fat mobilisation from fat cells (lipolysis).
Cortisone also promotes glucagon release. Glucagon is the so-called antagonist of the hormone insulin. Glucagon is released from the pancreas into the blood after a protein-rich meal or when the blood sugar level drops, and causes the blood sugar level to rise.
By stimulating the action of glucagon, cortisone also causes an increase in blood sugar levels. Furthermore, cortisone also has a direct inhibitory effect on cellular sugar uptake, causing the sugar level in the blood to rise and inhibiting the release of insulin. Insulin can then no longer reduce blood sugar levels.
Since cortisone is able to increase the blood sugar level, treatment with cortisone can promote a diabetic metabolic situation with high blood sugar concentrations. The andrenogenital syndrome is an inherited metabolic disorder in which there is a disturbance in hormone production in the adrenal cortex and is manifested by masculinization in girls or premature sexual development in boys and disturbances in the salt balance with fluid loss. The formation of cortisone and aldosterone (thirst hormone) is disturbed in andrenogenital syndrome.
Due to the lack of cortisone, the central control system in the brain (hypothalamus and pituitary gland) attempts to stimulate the adrenal gland compensatory by increasing the release of corticotropin by the pituitary gland. Corticotropin stimulates the adrenal cortex to produce its hormones. This ultimately leads to the complete exhaustion of the formation of cortisone in the adrenal cortex. Drug administration of cortisone remedies the lack of cortisone in the blood, the pituitary gland stops producing corticotropin, the adrenal cortex recovers and the symptoms caused by the cortisone deficiency disappear.
