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{{DrugProjectFormSinglePage
…{{drugbox
|authorTag={{DB}}
| IUPAC_name = 11,17,21-trihydroxy-,(11beta)-<BR>pregn-4-ene-3,20-dione
|genericName=Cortisol
| image = cortisol-2D-skeletal.png
|aOrAn=a
| image2 = cortisol-3D-vdW.png
|drugClass=anti-inflammatory agent
| width = 225px
|indicationType=treatment
| CAS_number = 50-23-7
|indication=itching associated with minor skin irritations and rashes due to [[eczema]], insect bites, soaps and detergents, cosmetics, jewelry, [[seborrheic dermatitis]], [[psoriasis]], poison ivy, oak or sumac and for external genital, feminine and anal itching
| ATC_prefix = H02
|blackBoxWarningTitle=Title
| ATC_suffix = AB09
|blackBoxWarningBody=<i><span style="color:#FF0000;">ConditionName: </span></i>
| ATC_supplemental = (and others)
| PubChem = 5754
| DrugBank =
| chemical_formula =
| C=21 | H=30 | O=5
| molecular_weight = 362.465
| bioavailability =
| protein_bound =
| metabolism =
| elimination_half-life =
| pregnancy_category = C
| legal_status =  
| routes_of_administration = Oral tablets, intravenously, topical
}}
{{SI}}
__NOTOC__
{{GS}}


* Content


<!--Adult Indications and Dosage-->


<!--FDA-Labeled Indications and Dosage (Adult)-->
|fdaLIADAdult=Uses:


*for temporary relief of itching associated with minor skin irritations and rashes due to:
'''Cortisol''' is a [[corticosteroid]] [[hormone]] produced by the [[adrenal cortex]] (in the adrenal gland). It is a vital hormone that is often referred to as the "stress hormone" as it  is involved in the response to [[stress (medicine)|stress]]. It increases [[blood pressure]], [[blood sugar]] levels and has an [[immunosuppressive]] action.  In [[pharmacology]], the synthetic form of cortisol is referred to as '''hydrocortisone''', and is used to treat [[allergy|allergies]] and [[inflammation]] as well as cortisol production deficiencies.  When first introduced as a treatment for rheumatoid arthritis, it was referred to as '''Compound E'''.
:*[[eczema]]
:*insect bites
:*soaps and detergents
:*cosmetics
:*jewelry
:*[[seborrheic dermatitis]]
:*[[psoriasis]]
:*poison ivy, oak or sumac
:*for external genital, feminine and anal [[itching]]
:*other uses of this product should be only under the advice and supervision of a doctor


*Dosing information
==Physiology==
===Diurnal variation===
The amount of cortisol present in the [[blood|serum]] undergoes diurnal variation, with the highest levels present in the early morning, and the lowest levels present around midnight, 3-5 hours after the onset of [[sleep]]. Information about the [[Circadian rhythm|light/dark cycle]] is transmitted from the [[retina]] to the paired [[suprachiasmatic nuclei]] in the [[hypothalamus]]. The pattern is not present at birth (estimates of when it starts vary from two weeks to 9 months.<ref>{{cite journal |author=de Weerth C, Zijl R, Buitelaar J |title=Development of cortisol circadian rhythm in infancy |journal=Early Hum Dev |volume=73 |issue=1-2 |pages=39-52 |year=2003 |pmid=12932892}}</ref>)


:* '''For minor skin irritations and [[rash]]es'''


:*adults: apply to affected area not more than 3 to 4 times daily.
Changed patterns of serum cortisol levels have been observed in connection with abnormal [[ACTH]] levels, [[clinical depression]], [[stress (psychology)|psychological stress]], and such physiological stressors as [[hypoglycemia]], illness, [[fever]], trauma, [[surgery]], [[fear]], [[Pain and nociception|pain]], physical exertion or extremes of temperature.  


:*'''For external anal itching:'''
There is also significant individual variation, although a given person tends to have consistent rhythms.


:*adults: when practical, cleanse the affected area with mild soap and warm water and rinse thoroughly
===Effects===
:*gently dry by patting or blotting with toilet tissue or soft cloth before application of this product.
:''See also [[Glucocorticoid#Medical uses and effects of high dose glucocorticoids|Medical uses and effects of high dose glucocorticoids]]''
|offLabelAdultGuideSupport=*There is limited information regarding <i>Off-Label Guideline-Supported Use</i> of {{PAGENAME}} in adult patients.
|offLabelAdultNoGuideSupport=*There is limited information regarding <i>Off-Label Non–Guideline-Supported Use</i> of Cortisol in adult patients.
|fdaLIADPed=Uses:


*for temporary relief of itching associated with minor skin irritations and rashes
In normal release, cortisol (like other [[glucocorticoid]] agents) has widespread actions which help restore [[homeostasis]] after [[Stress (medicine)|stress]]. (These normal [[endogenous]] functions are the basis for the physiological consequences of chronic stress - prolonged cortisol secretion.)


*Dosing information
* It acts as a physiological [[Receptor antagonist|antagonist]] to [[insulin]] by promoting [[glycogenolysis]] (breakdown of [[glycogen]]), breakdown of [[lipid]]s ([[lipolysis]]), and [[protein]]s, and mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating [[glucose]] concentrations (in the blood). There is a decreased [[glycogen]] formation in the [[liver]] . <ref>Freeman, Scott (2002). ''Biological Science''. Prentice Hall; 2nd Pkg edition (December 30, 2004). ISBN 0-13-218746-9.</ref> Prolonged cortisol secretion causes [[hyperglycemia]].


:*'''For minor skin irritations and rashes'''
* It can weaken the activity of the [[immune system]] . Cortisol prevents proliferation of T-cells by rendering the [[interleukin-2]] producer [[T-cell]]s unresponsive to [[interleukin-1]] (IL-1), and unable to produce the T-cell growth factor.<ref>{{cite journal |author=Palacios R., Sugawara I. |title=Hydrocortisone abrogates proliferation of T cells in autologous mixed lymphocyte reaction by rendering the interleukin-2 Producer T cells unresponsive to interleukin-1 and unable to synthesize the T-cell growth factor |journal=Scand J Immunol |volume=15 |issue=1 |pages=25-31 |year=1982 |pmid=6461917}}</ref> It reflects [[leukocyte]] redistribution to lymph nodes, [[bone marrow]], and [[skin]]. Acute 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.


:*children 2 years of age and older: apply to affected area not more than 3 to 4 times daily.
* It lowers [[bone]] formation thus favoring development of osteoporosis in the long term. Cortisol moves [[potassium]] into cells in exchange for an equal number of [[sodium]] ions.<ref>{{cite journal |author=Knight, R.P., Jr. Kornfield, D.S. Glaser, G.H. Bondy, P.K. |title=Effects of intravenous hydrocortisone on electrolytes of serum and urine in man |journal=J Clin Endocrinol Metab |volume=15 |issue=2 |pages=176-81 |year=1955 |pmid=13233328}}</ref> This can cause a major problem with the [[hyperkalemia]] of metabolic shock from surgery.


:*'''For external anal itching:'''
* It may help to create [[memories]] when exposure is short-term; this is the proposed mechanism for storage of [[flash bulb memories]]. However, long-term exposure to cortisol results in damage to cells in the [[hippocampus]]. This damage results in impaired learning.


:*adults: when practical, cleanse the affected area with mild soap and warm water and rinse thoroughly
* It increases [[blood pressure]] by increasing the sensitivity of the vasculature to epinephrine and norepinephrine.  In the absence of cortisol, widespread [[vasodilation]] occurs.


:*gently dry by patting or blotting with toilet tissue or soft cloth before application of this product
* It inhibits the secretion of [[corticotropin-releasing hormone]] (CRH), resulting in feedback inhibition of [[ACTH]] secretion. Some researchers believe that this normal feedback system may break down when animals are exposed to chronic stress.


:*children : under 12 years of age, consult a doctor.
* It increases the effectiveness of [[catecholamine]]s.
|offLabelPedGuideSupport=*There is limited information regarding <i>Off-Label Guideline-Supported Use</i> of Cortisol in pediatric patients.
|offLabelPedNoGuideSupport=*There is limited information regarding <i>Off-Label Non–Guideline-Supported Use</i> of Cortisol in pediatric patients.
|clinicalTrials=*There is limited information regarding <i>Clinical Trial Experience</i> of {{PAGENAME}} in the drug label.
|postmarketing=*There is limited information regarding <i>Postmarketing Experience</i> of {{PAGENAME}} in the drug label.


* It allows for the kidneys to produce [[hypotonic]] urine.


* It has anti-inflammatory effects by reducing [[histamine]] secretion and stabilizing [[lysosome|lysosomal]] membranes.  The stabilization of lysosomal membranes prevents their rupture, thereby preventing damage to healthy tissues.


* It stimulates hepatic [[detoxification]] by inducing tryptophan oxygenase (to reduce [[serotonin]] levels in the brain), glutamine synthase (reduce [[glutamate]] and [[ammonia]] levels in the brain), cytochrome P-450 hemoprotein (mobilizes [[arachidonic acid]]), and metallothionein (reduces [[heavy metals]] in the body).


<!--Drug Interactions-->
In addition to the effects caused by cortisol binding to the [[glucocorticoid receptor]], because of its molecular similarity to [[aldosterone]], it also binds to the [[mineralocorticoid receptor]]. (It binds with less affinity to it than aldosterone does, but the concentration of blood cortisol is higher than that of blood aldosterone.)
|useInPregnancyAUS=* '''Australian Drug Evaluation Committee (ADEC) Pregnancy Category'''


There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of {{PAGENAME}} in women who are pregnant.
===Binding===
|useInLaborDelivery=*There is no FDA guidance on use of {{PAGENAME}} during labor and delivery.
Most serum cortisol, all but about 4%, is bound to proteins including [[Transcortin|corticosteroid binding globulin]] ('''CBG'''), and [[serum albumin]]. Only free cortisol is available to most receptors.
|useInNursing=*There is no FDA guidance on the use of {{PAGENAME}} with respect to nursing mothers.
|useInPed=*There is no FDA guidance on the use of {{PAGENAME}} with respect to pediatric patients.
|useInGeri=*There is no FDA guidance on the use of {{PAGENAME}} with respect to geriatric patients.
|useInGender=*There is no FDA guidance on the use of {{PAGENAME}} with respect to specific gender populations.
|useInRace=*There is no FDA guidance on the use of {{PAGENAME}} with respect to specific racial populations.
|useInRenalImpair=*There is no FDA guidance on the use of {{PAGENAME}} in patients with renal impairment.
|useInHepaticImpair=*There is no FDA guidance on the use of {{PAGENAME}} in patients with hepatic impairment.
|useInReproPotential=*There is no FDA guidance on the use of {{PAGENAME}} in women of reproductive potentials and males.
|useInImmunocomp=*There is no FDA guidance one the use of {{PAGENAME}} in patients who are immunocompromised.


<!--Administration and Monitoring-->
==Diseases and disorders==
|administration=Directions:


*For minor skin irritations and rashes,
* '''Hypercortisolism''': Excessive levels of cortisol in the blood result in [[Cushing's syndrome]].


:*adults and children 2 years of age and older: apply to affected area not more than 3 to 4 times daily.  
* '''Hypocortisolism, or [[adrenal insufficiency]]''': If on the other hand the adrenal glands do not produce sufficient amounts of cortisol, [[Addison's disease]] is the consequence.


*For external anal itching:
The relationship between cortisol and ACTH is as follows:


:*adults: when practical, cleanse the affected area with mild soap and warm water and rinse thoroughly
{| class="wikitable"
:*gently dry by patting or blotting with toilet tissue or soft cloth before application of this product
|+ THE DISORDERS OF CORTISOL SECRETION<!-- -->
:*children : under 12 years of age, consult a doctor.
!
! Plasma Cortisol
! Plasma ACTH
|-
| '''Primary Hypercortisolism''' ([[Cushing's syndrome]])
| ↑
| ↓
|-
| '''Secondary Hypercortisolism''' (pituitary, Cushing's disease)
| ↑
| ↑
|-
| '''Primary Hypocortisolism''' (Addison's disease)
| ↓
| ↑
|-
| '''Secondary Hypocortisolism''' (pituitary)
| ↓
| ↓
|}


*Other information:
==Pharmacology==
Hydrocortisone is the chemical form of cortisol used for oral administration or intravenous injection. It is used as an [[immunosuppressive drug]], given by injection in the treatment of severe allergic reactions such as [[anaphylaxis]] and [[angioedema]], in place of [[prednisolone]] in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an [[Addison's disease|Addisonian crisis]].


:*do not use if seal is punctured or is not visible. To open, reverse cap to puncture seal
It is given by topical application for its [[anti-inflammatory]] effect in allergic rashes, [[eczema]], [[psoriasis]] and certain other inflammatory conditions. 
:*store at room temperature
:*see crimp of tube for Lot Number and Expiration Date
|monitoring=*There is limited information regarding <i>Monitoring</i> of {{PAGENAME}} in the drug label.
|IVCompat=*There is limited information regarding <i>IV Compatibility</i> of {{PAGENAME}} in the drug label.
|drugBox=[[File:Hydrocortisone image.png|600px|thumbnail|left]]
{{clear}}
|structure=*


: [[File:{{PAGENAME}}01.png|thumb|none|600px|This image is provided by the National Library of Medicine.]]
It may also be injected into inflamed joints resulting from diseases such as [[gout]].
|PD=*There is limited information regarding <i>Pharmacodynamics</i> of {{PAGENAME}} in the drug label.
|PK=*There is limited information regarding <i>Pharmacokinetics</i> of {{PAGENAME}} in the drug label.
|nonClinToxic=*There is limited information regarding <i>Nonclinical Toxicology</i> of {{PAGENAME}} in the drug label.
|clinicalStudies=*There is limited information regarding <i>Clinical Studies</i> of {{PAGENAME}} in the drug label.
|drugImages=[[File:Hydrocortisone pdp.png|600px|thumbnail|left]]
{{clear}}


[[File:Hydrocortisone pdp2.png|600px|thumbnail|left]]
Compared to [[prednisolone]], hydrocortisone is about 1/4th the strength (for the [[anti-inflammatory]] effect only). [[Dexamethasone]] is about 40 times stronger than hydrocortisone. For side effects, see [[corticosteroid]] and [[prednisolone]]. Non prescription 1% hydrocortisone cream or ointment are available; stronger forms are prescription only.[http://www.drnase.com/Prescipt_ions_non.htm]
{{clear}}


[[File:Hydrocortisone label.png|600px|thumbnail|left]]
==Biochemistry==
{{clear}}
===Biosynthesis===
|fdaPatientInfo=*There is limited information regarding <i>Patient Counseling Information</i> of {{PAGENAME}} in the drug label.
Cortisol is synthesized from [[cholesterol]]. The synthesis takes place in the ''[[zona fasciculata]]'' of the [[adrenal cortex|cortex of the adrenal glands]]. (The name ''cortisol'' comes from ''cortex''.) While the adrenal cortex also produces [[aldosterone]] (in the ''zona glomerulosa'') and some [[sex hormone]]s (in the ''zona reticularis''), cortisol is its main secretion. The medulla of the adrenal gland lies under the cortex and mainly secretes the catecholamines, adrenaline (epinephrine) and noradrenaline (norepinephrine) under sympathetic stimulation (more epinephrine is produced than norepinephrine, in a ratio 4:1).


<!--Precautions with Alcohol-->
The synthesis of cortisol in the adrenal gland is stimulated by the [[anterior pituitary|anterior lobe]] of the [[pituitary gland]] with [[adrenocorticotropic hormone]] (ACTH); production of ACTH is in turn stimulated by [[corticotropin-releasing hormone]] (CRH), released by the [[hypothalamus]]. ACTH increases the concentration of cholesterol in the inner mitochondrial membrane (via regulation of STAR (steroidogenic acute regulatory) protein). The cholesterol is converted to pregnenolone, catalysed by Cytochrome P450SCC (side chain cleavage).
|alcohol=* Alcohol-{{PAGENAME}} interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.


<!--Brand Names-->
=== Metabolism ===
|brandNames=* ®<ref>{{Cite web | title =  | url =  }}</ref>
Cortisol is metabolized by the [[11-beta hydroxysteroid dehydrogenase]] system (11-beta HSD), which consists of two enzymes: [[11-beta HSD1]] and [[11-beta HSD2]].
* ''11-beta HSD1'' utilizes the cofactor NADPH to convert biologically inert cortisone to biologically active cortisol.
* ''11-beta HSD2'' utilizes the cofactor NAD+ to convert cortisol to cortisone.


<!--Look-Alike Drug Names-->
Overall the net effect is that 11-beta HSD1 serves to increase the local concentrations of biologically active cortisol in a given tissue, while 11-beta HSD2 serves to decrease the local concentrations of biologically active cortisol.
|lookAlike=* A® — B®<ref name="www.ismp.org">{{Cite web  | last =  | first =  | title = http://www.ismp.org | url = http://www.ismp.org | publisher =  | date =  }}</ref>
 
<!--Drug Shortage Status-->
|drugShortage=
}}
{{PillImage
|fileName=No image.jpg
}}
{{LabelImage
|fileName={{PAGENAME}}11.png
}}
{{LabelImage
|fileName={{PAGENAME}}11.png
}}
<!--Pill Image-->


An alteration in 11-beta HSD1 has been suggested to play a role in the [[pathogenesis]] of [[obesity]], [[hypertension]], and [[insulin resistance]], sometimes referred to the [[metabolic syndrome]].


An alteration in 11-beta HSD2 has been implicated in [[essential hypertension]] and is known to lead to the [[syndrome of apparent mineralocorticoid excess]] (SAME).


<!--Label Display Image-->
== See also ==
* [[Cushing's syndrome]]
* [[HPA axis]]
* [[Hypopituitarism]]
* [[Post-traumatic stress disorder]]
* [[Central serous retinopathy]]
* [[CortiSlim]]
* [[Relacore]], a pill which claims to reduce Cortisol.


==Additional images==
<gallery>
Image:Steroidogenesis.gif|[[Steroidogenesis]]
Image:11-Deoxycortisol.png|[[11-Deoxycortisol]]
</gallery>


==References==
<references/>


==External links==


{{Hormones}}
{{Corticosteroids}}
{{Antidiarrheals, intestinal anti-inflammatory/anti-infective agents}}
{{Otologicals}}


<!--Category-->
[[Category:Glucocorticoids]]
[[Category:Immunosuppressive agents]]
[[Category:Endocrinology]]
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{{WikiDoc Sources}}


[[Category:Drug]]
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[[fr:Cortisol]]
[[he:קורטיזול]]
[[nl:Cortisol]]
[[ja:コルチゾール]]
[[no:Kortisol]]
[[pl:Kortyzol]]
[[pt:Cortisol]]
[[sl:Kortizol]]
[[fi:Kortisoli]]
[[sv:Kortisol]]
[[tr:Kortizol]]

Latest revision as of 20:16, 7 May 2015

…

Cortisol
Clinical data
Pregnancy
category
  • C
Routes of
administration		Oral tablets, intravenously, topical
ATC code
Identifiers
CAS Number
PubChem CID
E number{{#property:P628}}
ECHA InfoCard{{#property:P2566}}Lua error in Module:EditAtWikidata at line 36: attempt to index field 'wikibase' (a nil value).
Chemical and physical data
FormulaC21H30O5
Molar mass362.465

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-632-7753



Cortisol is a corticosteroid hormone produced by the adrenal cortex (in the adrenal gland). It is a vital hormone that is often referred to as the "stress hormone" as it is involved in the response to stress. It increases blood pressure, blood sugar levels and has an immunosuppressive action. In pharmacology, the synthetic form of cortisol is referred to as hydrocortisone, and is used to treat allergies and inflammation as well as cortisol production deficiencies. When first introduced as a treatment for rheumatoid arthritis, it was referred to as Compound E.

Physiology

Diurnal variation

The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning, and the lowest levels present around midnight, 3-5 hours after the onset of sleep. Information about the light/dark cycle is transmitted from the retina to the paired suprachiasmatic nuclei in the hypothalamus. The pattern is not present at birth (estimates of when it starts vary from two weeks to 9 months.[1])


Changed patterns of serum cortisol levels have been observed in connection with abnormal ACTH levels, clinical depression, psychological stress, and such physiological stressors as hypoglycemia, illness, fever, trauma, surgery, fear, pain, physical exertion or extremes of temperature.

There is also significant individual variation, although a given person tends to have consistent rhythms.

Effects

See also Medical uses and effects of high dose glucocorticoids

In normal release, cortisol (like other glucocorticoid agents) has widespread actions which help restore homeostasis after stress. (These normal endogenous functions are the basis for the physiological consequences of chronic stress - prolonged cortisol secretion.)

  • It 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.[3] It reflects leukocyte redistribution to lymph nodes, bone marrow, and skin. Acute 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.
  • It lowers bone formation thus favoring development of osteoporosis in the long term. Cortisol moves potassium into cells in exchange for an equal number of sodium ions.[4] This can cause a major problem with the hyperkalemia of metabolic shock from surgery.
  • It may help to create memories when exposure is short-term; this is the proposed mechanism for storage of flash bulb memories. However, long-term exposure to cortisol results in damage to cells in the hippocampus. This damage results in impaired learning.
  • It increases blood pressure by increasing the sensitivity of the vasculature to epinephrine and norepinephrine. In the absence of cortisol, widespread vasodilation occurs.
  • It inhibits the secretion of corticotropin-releasing hormone (CRH), resulting in feedback inhibition of ACTH secretion. Some researchers believe that this normal feedback system may break down when animals are exposed to chronic stress.
  • It allows for the kidneys to produce hypotonic urine.
  • It has anti-inflammatory effects by reducing histamine secretion and stabilizing lysosomal membranes. The stabilization of lysosomal membranes prevents their rupture, thereby preventing damage to healthy tissues.

In addition to the effects caused by cortisol binding to the glucocorticoid receptor, because of its molecular similarity to aldosterone, it also binds to the mineralocorticoid receptor. (It binds with less affinity to it than aldosterone does, but the concentration of blood cortisol is higher than that of blood aldosterone.)

Binding

Most serum cortisol, all but about 4%, is bound to proteins including corticosteroid binding globulin (CBG), and serum albumin. Only free cortisol is available to most receptors.

Diseases and disorders

The relationship between cortisol and ACTH is as follows:

THE DISORDERS OF CORTISOL SECRETION
Plasma Cortisol Plasma ACTH
Primary Hypercortisolism (Cushing's syndrome) ↑ ↓
Secondary Hypercortisolism (pituitary, Cushing's disease) ↑ ↑
Primary Hypocortisolism (Addison's disease) ↓ ↑
Secondary Hypocortisolism (pituitary) ↓ ↓

Pharmacology

Hydrocortisone is the chemical form of cortisol used for oral administration or intravenous injection. It is used as an immunosuppressive drug, given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis.

It is given by topical application for its anti-inflammatory effect in allergic rashes, eczema, psoriasis and certain other inflammatory conditions.

It may also be injected into inflamed joints resulting from diseases such as gout.

Compared to prednisolone, hydrocortisone is about 1/4th the strength (for the anti-inflammatory effect only). Dexamethasone is about 40 times stronger than hydrocortisone. For side effects, see corticosteroid and prednisolone. Non prescription 1% hydrocortisone cream or ointment are available; stronger forms are prescription only.[2]

Biochemistry

Biosynthesis

Cortisol is synthesized from cholesterol. The synthesis takes place in the zona fasciculata of the cortex of the adrenal glands. (The name cortisol comes from cortex.) While the adrenal cortex also produces aldosterone (in the zona glomerulosa) and some sex hormones (in the zona reticularis), cortisol is its main secretion. The medulla of the adrenal gland lies under the cortex and mainly secretes the catecholamines, adrenaline (epinephrine) and noradrenaline (norepinephrine) under sympathetic stimulation (more epinephrine is produced than norepinephrine, in a ratio 4:1).

The synthesis of cortisol in the adrenal gland is stimulated by the anterior lobe of the pituitary gland with adrenocorticotropic hormone (ACTH); production of ACTH is in turn stimulated by corticotropin-releasing hormone (CRH), released by the hypothalamus. ACTH increases the concentration of cholesterol in the inner mitochondrial membrane (via regulation of STAR (steroidogenic acute regulatory) protein). The cholesterol is converted to pregnenolone, catalysed by Cytochrome P450SCC (side chain cleavage).

Metabolism

Cortisol is metabolized by the 11-beta hydroxysteroid dehydrogenase system (11-beta HSD), which consists of two enzymes: 11-beta HSD1 and 11-beta HSD2.

  • 11-beta HSD1 utilizes the cofactor NADPH to convert biologically inert cortisone to biologically active cortisol.
  • 11-beta HSD2 utilizes the cofactor NAD+ to convert cortisol to cortisone.

Overall the net effect is that 11-beta HSD1 serves to increase the local concentrations of biologically active cortisol in a given tissue, while 11-beta HSD2 serves to decrease the local concentrations of biologically active cortisol.

An alteration in 11-beta HSD1 has been suggested to play a role in the pathogenesis of obesity, hypertension, and insulin resistance, sometimes referred to the metabolic syndrome.

An alteration in 11-beta HSD2 has been implicated in essential hypertension and is known to lead to the syndrome of apparent mineralocorticoid excess (SAME).

See also

Additional images

References

  1. ↑ de Weerth C, Zijl R, Buitelaar J (2003). "Development of cortisol circadian rhythm in infancy". Early Hum Dev. 73 (1–2): 39–52. PMID 12932892.
  2. ↑ Freeman, Scott (2002). Biological Science. Prentice Hall; 2nd Pkg edition (December 30, 2004). ISBN 0-13-218746-9.
  3. ↑ Palacios R., Sugawara I. (1982). "Hydrocortisone abrogates proliferation of T cells in autologous mixed lymphocyte reaction by rendering the interleukin-2 Producer T cells unresponsive to interleukin-1 and unable to synthesize the T-cell growth factor". Scand J Immunol. 15 (1): 25–31. PMID 6461917.
  4. ↑ Knight, R.P., Jr. Kornfield, D.S. Glaser, G.H. Bondy, P.K. (1955). "Effects of intravenous hydrocortisone on electrolytes of serum and urine in man". J Clin Endocrinol Metab. 15 (2): 176–81. PMID 13233328.

External links

Template:Corticosteroids Template:Antidiarrheals, intestinal anti-inflammatory/anti-infective agents Template:Otologicals

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