Not to be confused with
cortisone, a similar compound with a similar name, genesis, and function.
Cortisol
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Other effects[edit]
Cortisol is released in response to stress, sparing available glucose for the brain, generating new energy from stored reserves, and diverting energy from low-priority activities (such as the immune system) in order to survive immediate threats or prepare for the exertion of rising to a new day. However, prolonged cortisol secretion (which may be due to
chronic stress or the excessive secretion seen in
Cushing's syndrome) results in significant physiological changes.
[1]
- Insulin
- Collagen
In laboratory rats, cortisol-induced collagen loss in the skin is ten times greater than in any other tissue.
[18]
- Amino acids
Cortisol raises the free amino acids in the serum. It does this by inhibiting collagen formation, decreasing amino acid uptake by muscle, and inhibiting protein synthesis.
[19] Cortisol (as opticortinol) may inversely inhibit
IgA precursor cells in the intestines of calves.
[20]Cortisol also inhibits IgA in serum, as it does
IgM; however, it is not shown to inhibit
IgE.
[21]
- Gastric and renal secretion
Cortisol stimulates gastric-acid secretion.
[22] Cortisol's only direct effect on the hydrogen ion excretion of the kidneys is to stimulate the excretion of ammonium ions by deactivating the renal glutaminase enzyme.
[23] Net chloride secretion in the intestines is inversely decreased by cortisol
in vitro (
methylprednisolone).
[24]
- Sodium
Cortisol inhibits sodium loss through the small intestine of mammals.
[25] Sodium depletion, however, does not affect cortisol levels
[26]so cortisol cannot be used to regulate serum sodium. Cortisol's original purpose may have been sodium transport. This hypothesis is supported by the fact that freshwater fish utilize cortisol to stimulate sodium inward, while saltwater fish have a cortisol-based system for expelling excess sodium.
[27]
- Potassium
A sodium load augments the intense potassium excretion by cortisol;
corticosterone is comparable to cortisol in this case.
[17] For potassium to move out of the cell, cortisol moves an equal number of sodium ions into the cell.
[28] This should make
pH regulation much easier (unlike the normal potassium-deficiency situation, in which two sodium ions move in for each three potassium ions that move out—closer to the
deoxycorticosterone effect). Nevertheless, cortisol consistently causes serum
alkalosis; in a deficiency, serum pH does not change. The purpose of this may be to reduce serum pH to an optimum value for some immune enzymes during infection, when cortisol declines. Potassium is also blocked from loss in the kidneys by a decline in cortisol (9 alpha fluorohydrocortisone).
[29]
- Water
Cortisol acts as anti- diuretic hormone, controlling one-half of intestinal diuresis;
[25] it has also been shown to control kidney diuresis in dogs. The decline in water excretion following a decline in cortisol (dexamethasone) in dogs is probably due to inverse stimulation of
antidiuretic hormone (ADH or
arginine vasopressin), which is not overridden by water loading.
[30] Humans and other animals also use this mechanism.
[31]
- Copper
Cortisol stimulates many copper enzymes (often to 50% of their total potential), probably to increase copper availability for immune purposes.
[32]:337 This includes lysyl oxidase, an enzyme that cross-links collagen and
elastin.
[32]:334 Especially valuable for immune response is cortisol's stimulation of the
superoxide dismutase,
[33] since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria. Cortisol causes an inverse four- or fivefold decrease of
metallothionein (a copper storage protein) in mice;
[34] however, rodents do not synthesize cortisol themselves. This may be to furnish more copper for ceruloplasmin synthesis or to release free copper. Cortisol has an opposite effect on aminoisobuteric acid than on the other amino acids.
[35] If alpha-aminoisobuteric acid is used to transport copper through the cell wall, this anomaly might be explained.
- Immune system
Cortisol can weaken the activity of the
immune system. Cortisol prevents proliferation of T-cells by rendering the
interleukin-2 producer
T-cells unresponsive to
interleukin-1 (IL-1), and unable to produce the T-cell growth factor.
[36] Cortisol also has a negative-feedback effect on interleukin-1.
[37] IL-1 must be especially useful in combating some diseases; however,
endotoxic bacteria have gained an advantage by forcing the
hypothalamus to increase cortisol levels (forcing the secretion of
CRH hormone, thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor (GRMF),
[38] so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes (reflecting
leukocyte redistribution to lymph nodes,
bone marrow, and
skin). Rapid administration of
corticosterone (the endogenous Type I and Type II receptor agonist) or
RU28362 (a specific Type II receptor agonist) to adrenalectomized animals induced changes in
leukocyte distribution.
Natural killer cells are not affected by cortisol.
[39]
- Bone metabolism
Cortisol reduces
bone formation, favoring long-term development of osteoporosis. It transports
potassium out of cells in exchange for an equal number of
sodium ions (see above).
[28] This can trigger the
hyperkalemia of
metabolic shock from surgery. Cortisol also reduces
calcium absorption in the intestine.
[40]
- Memory
Cortisol works with
epinephrine (adrenaline) to create
memories of short-term emotional events; this is the proposed mechanism for storage of
flash bulb memories, and may originate as a means to remember what to avoid in the future.
[41] However, long-term exposure to cortisol damages cells in the
hippocampus;
[42] this damage results in impaired learning. Furthermore, it has been shown that cortisol inhibits memory retrieval of already stored information.
[43][44]
- Additional effects
- Shuts down the reproductive system, resulting in an increased chance of miscarriage and (in some cases) temporary infertility. Fertility returns after cortisol levels return to normal.[46]
- Has anti-inflammatory properties, reducing histamine secretion and stabilizing lysosomal membranes. Stabilization of lysosomal membranes prevents their rupture, preventing damage to healthy tissues[47]
- In addition to cortisol's effects in binding to the glucocorticoid receptor, because of its molecular similarity to aldosterone it also binds to the mineralocorticoid receptor. Aldosterone and cortisol have a 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 and allow selective mineralocorticoid action. This enzyme—11-beta hydroxysteroid dehydrogenase type II (Protein:HSD11B2)—catalyzes the deactivation of glucocorticoids to 11-dehydro metabolites[48]
- There are potential links between cortisol, appetite and obesity.[49] "
