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Aldosterone

Aldosterone is a steroid hormone (mineralocorticoid

family) produced by the outer section (zona glomerulosa)

of theadrenal cortexin theadrenal gland.[1][2] It plays

a central role in the regulation of blood pressure mainly

by acting on thedistal tubulesandcollecting ductsof the

nephron, increasing reabsorption of ions and water in the

kidney, to cause the conservation ofsodium, secretion

ofpotassium, increase in water retention, and increase

inblood pressure and blood volume.[1] When dysregu-

lated, aldosterone is pathogenic and contributes to the

development and progression of cardiovascular and renaldisease.[2] Aldosterone has exactly the opposite function

of theatrial natriuretic hormonesecreted by theheart.[1]

Drugs that interfere with the secretion or action of al-

dosterone are in use as antihypertensives, likelisinopril,

which lowers blood pressure by blocking theangiotensin-

converting enzyme(ACE), leading to lower aldosterone

secretion. The net effect of these drugs is to reduce

sodium and water retention but increase retention of

potassium. Aldosterone is part of the renin-angiotensin

system. Another example isspironolactone, a potassium-

sparing diuretic, which decreases blood pressure by re-

leasing fluid from the body while retaining potassium.It was first isolated bySimpsonand Tait in 1953.[3]

1 Synthesis

The corticosteroids are synthesized from cholesterol

within the zona glomerulosa of adrenal cortex. Most

steroidogenicreactions are catalysed by enzymes of the

cytochrome P450 family. They are located within themitochondriaand requireadrenodoxinas a cofactor (ex-

cept21-hydroxylaseand 17-hydroxylase).

Aldosterone and corticosterone share the first part of their

biosynthetic pathways. The last parts are mediated ei-

ther by thealdosterone synthase(for aldosterone) or by

the 11-hydroxylase (for corticosterone). These enzymes

are nearly identical (they share 11-hydroxylation and18-

hydroxylationfunctions), but aldosterone synthase is also

able to perform an 18-oxidation. Moreover, aldosterone

synthase is found within the zona glomerulosa at the outer

edge of theadrenal cortex; 11-hydroxylase is found in

thezona fasciculataandreticularis.Note: aldosterone synthaseis absent in other sections of

theadrenal gland.

H

HH

HO

O

O

OH

HO

O

O

OH

HO OH

O

HO

O

OH

HO

O

HO

O

O

OH

O

O

OH

OH

O

HO

HO

OH

O

O

O

O

OH

O

O

O

OH

OH

OH

Cholesterol

Pregnenolone

Progesterone Deoxy-

corticosterone

Corticosterone

17-hydroxypregnenolone

17-hydroxyprogesterone 11-deoxycortisol

Cortisol

Dehydroepi-androsterone

Androste-nedione

Estrone

Androstenediol Testosterone Estradiol

Dihydrotestosterone

12

34 5 6

7

8

9

10

11

12

13

14

15

16

17

18

19

2021 22

23

24

25

26

27

Estriol

HO

OH

OH

Cellular location

Mitochondria

Smooth endoplasmic

reticulum

3-beta-hydroxysteroiddehydrogenase(3-HSD)

17-hydroxylase

17,20 lyase

17-HSD

(liver

an

dplacenta)

21-hydroxylase

Aromatase

11-hydroxylase

5-reductase

Progestagens(21carbons)

OH

HO

Androgens(19carbons)

Estro

gens(1

8carb

ons)

Glucocorticoids

(21 carbons)

Aldosterone

synthase

Mineralocorticoids

(21 carbons)

of enzymes

Cholesterol side-chain

cleavage enzyme

AldosteroneO

HO

OO

OH

Steroidogenesis, showing aldosterone synthesis at upper-right

corner

1.1 Stimulation

Aldosterone synthesis is stimulated by several factors:

increase in the plasma concentration of angiotensin

III, a metabolite of angiotensin II

increase in plasma angiotensin II, ACTH, or

potassiumlevels, which are present in proportion to

plasma sodium deficiencies. (The increased potas-

sium level works to regulate aldosterone synthesis

by depolarizing the cells in the zona glomerulosa,

which opens the voltage-dependent calcium chan-

nels.) The level of angiotensin II is regulated by

angiotensin I, which is in turn regulated by renin,

an enzyme secreted in the kidneys. Potassium levelsare the most sensitive stimulator of aldosterone.

the ACTH stimulation test, which is sometimes used

to stimulate the production of aldosterone along

with cortisolto determine whether primary or sec-

ondary adrenal insufficiency is present. However,

ACTH has only a minor role in regulating aldos-

terone production; with hypopituitarism there is no

atrophy of the zona glomerulosa.

plasmaacidosis

thestretch receptorslocated in theatriaof the heart.

If decreased blood pressure is detected, the adrenal

1
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2 4 CONTROL OF ALDOSTERONE RELEASE FROM THE ADRENAL CORTEX

gland is stimulated by these stretch receptors to re-

lease aldosterone, which increases sodium reabsorp-

tion from the urine, sweat, and the gut. This causes

increased osmolarity in the extracellular fluid, which

will eventually return blood pressure toward normal.

adrenoglomerulotropin, a lipid factor, obtained from

pineal extracts. It selectively stimulates secretion of

aldosterone.[4]

The secretion of aldosterone has adiurnalrhythm.[5]

2 Function

Aldosterone is the primary of several endogenous mem-

bers of the class of mineralocorticoids in humans.

Deoxycorticosterone is another important member of thisclass. Aldosterone tends to promote Na+ and water reten-

tion, and lower plasma K+ concentration by the following

mechanisms:

1. Acting on the nuclearmineralocorticoid receptors

(MR) within the principal cells of thedistal tubule

and the collecting duct of the kidney nephron, it

upregulates and activates the basolateral Na+/K+

pumps, which pumps three sodium ions out of the

cell, into the interstitial fluid and two potassium ions

into the cell from the interstitial fluid. This cre-

ates a concentration gradient which results in reab-

sorption of sodium (Na+) ions and water (which fol-

lows sodium) into the blood, and secreting potas-

sium (K+) ions into the urine (lumen of collecting

duct).

2. Aldosterone upregulates epithelial sodium channels

(ENaCs), increasing apical membrane permeability

for Na+.

3. Cl is reabsorbed in conjunction with sodium

cations to maintain the systems electrochemical bal-

ance.

4. Aldosterone stimulates the secretion of K+

into thetubular lumen.[6]

5. Aldosterone stimulates Na+ and water reabsorption

from the gut, salivary and sweat glands in exchange

for K+.

6. Aldosterone stimulates secretion of H+ in exchange

for K+ in the intercalated cellsof the cortical collect-

ing tubules, regulating plasmabicarbonate(HCO3)

levels and its acid/base balance.[7]

Aldosterone is responsible for the reabsorption of about

2% of filtered sodium in the kidneys, which is nearlyequal to the entire sodium content in human blood un-

der normalglomerular filtration rates.[8]

Aldosterone, probably acting through mineralocorticoid

receptors, may positively influence neurogenesis in the

dentate gyrus.[9]

3 Location of receptors

Steroidreceptors are intracellular. The aldosterone min-

eralcorticoid receptor complex binds on the DNA to spe-

cifichormone response element, which leads to gene spe-

cifictranscription.

Some of the transcribed genes are crucial for transepithe-

lial sodium transport, including the threesubunitsof the

epithelial sodium channel (ENaC), the Na+/K+ pumps

and their regulatory proteinsserum and glucocorticoid-

induced kinase, and channel-inducing factor, respec-

tively.

The mineralcorticoid receptor is stimulated by both al-

dosterone and cortisol, but a mechanism protects the

body from excess aldosterone receptor stimulation by

glucocorticoids (such as cortisol), which happen to be

present at much higher concentrations than mineralcorti-

coids in the healthy individual. The mechanism consists

of an enzyme called11 -hydroxysteroid dehydrogenase

(11 -HSD). This enzyme co-localizes with intracellular

adrenal steroid receptors and converts cortisol into corti-

sone, a relatively inactive metabolite with little affinity for

the MR. Liquorice, which contains glycyrrhetinic acid,

can inhibit 11 -HSD and lead to a mineralcorticoid ex-

cess syndrome.

4 Control of aldosterone release

from the adrenal cortex

4.1 Major regulators

4.1.1 The role of the renin-angiotensin system

Angiotensin is involved in regulating aldosterone and is

the core regulation.[11] Angiotensin II acts synergisticallywith potassium, and the potassium feedback is virtu-

ally inoperative when no angiotensin II is present.[12] A

small portion of the regulation resulting from angiotensin

II must take place indirectly from decreased blood flow

through the liver due to constriction of capillaries.[13]

When the blood flow decreases so does the destruction

of aldosterone by liver enzymes.

Although sustained production of aldosterone requires

persistent calcium entry through low-voltage-activated

Ca2+ channels, isolated zona glomerulosa cells are consid-

ered nonexcitable, with recorded membrane voltages that

are too hyperpolarized to permitCa2+ channels entry.[2]However, mouse zona glomerulosa cells within adrenal

slices spontaneously generate membrane potential os-
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4.3 Aldosterone feedback 3

Renin-angiotensin-aldosterone system

Angiotensinogen

ReninAngiotensin I

Angiotensin II

Liver

Kidneys

AdrenalsAldosterone

+Thirst+Antidiuretic hormone

-

Na excretion

H O excretion2

--

+

Vasoconstriction of

blood vessels

Hypothalamus of brain

Pituitary gland

Corticotropin-releasing hormone

ACTH

K excretion+

+

High plasma K+

+Effectivecirculating

volume

+Extracellular

fluid

volume

Blood

pressure+

-

+

+

ACEin lungs

The renin-angiotensin system, showing role of aldosterone be-

tween theadrenal glandsand thekidneys[10]

cillations of low periodicity; this innate electrical ex-

citability of zona glomerulosa cells provides a platform

for the production of a recurrent Ca2+ channels signal

that can be controlled by angiotensin II and extracel-lular potassium, the 2 major regulators of aldosterone

production.[2] Voltage-gated Ca2+ channels have been de-

tected in the zona glomerulosa of the human adrenal,

which suggests thatCa2+ channel blockersmay directly

influence the adrenocortical biosynthesis of aldosterone

in vivo. [14]

4.1.2 The plasma concentration ofpotassium

The amount of aldosterone secreted is a direct function

of the serum potassium[15][16] as probably determined by

sensors in the carotid artery.[17][18]

4.1.3 ACTH

ACTH, a pituitary peptide, also has some stimu-

lating effect on aldosterone, probably by stimulat-

ing the formation of deoxycorticosterone, a precursor

of aldosterone.[19] Aldosterone is increased by blood

loss,[20] pregnancy,[21] and possibly by other circum-

stances such as physical exertion, endotoxin shock, and

burns.[22][23]

4.2 Miscellaneous regulators

4.2.1 The role ofsympathetic nerves

The aldosterone production is also affected to one extent

or another by nervous control, which integrates the in-

verse of carotid artery pressure,[17] pain, posture,[21] and

probably emotion (anxiety, fear, and hostility)[24] (includ-

ingsurgical stress).[25] Anxiety increases aldosterone,[24]

which must have evolved because of the time de-

lay involved in migration of aldosterone into the cell

nucleus.[26] Thus, there is an advantage to an animals an-

ticipating a future need from interaction with a predator,

since too high a serum content of potassium has very ad-

verse effects on nervous transmission.

4.2.2 The role ofbaroreceptors

Pressure-sensitive baroreceptors are found in the vesselwalls of nearly all large arteries in the thorax and neck,

but are particularly plentiful in the sinuses of the carotid

arteries and in the arch of the aorta. These specialized re-

ceptors are sensitive to changes in mean arterial pressure.

An increase in sensed pressure results in an increased rate

of firing by the baroreceptors and a negative feedback re-

sponse, lowering systemic arterial pressure. Aldosterone

release causes sodium and water retention, which causes

increased blood volume, and a subsequent increase in

blood pressure, which is sensed by the baroreceptors.[27]

To maintain normal homeostasis these receptors also de-

tect low blood pressure or low blood volume, causing al-dosterone to be released. This results in sodium retention

in the kidney, leading to water retention and increased

blood volume.[28]

4.2.3 The plasma concentration ofsodium

Aldosterone is a function of the inverse of the sodium in-

take as sensed via osmotic pressure.[29] The slope of the

response of aldosterone to serum potassium is almost in-

dependent of sodium intake.[30] Aldosterone is much in-

creased at low sodium intakes, but the rate of increase ofplasma aldosterone as potassium rises in the serum is not

much lower at high sodium intakes than it is at low. Thus,

the potassium is strongly regulated at all sodium intakes

by aldosterone when the supply of potassium is adequate,

which it usually is in primitive diets.

4.3 Aldosterone feedback

Feedback by aldosterone concentration itself is of a non-

morphological character (that is, other than changes inthe cells number or structure) and is poor, so the elec-

trolyte feedbacks predominate, short term.[22]
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4 8 REFERENCES

5 Associated clinical conditions

Hyperaldosteronism is abnormally increased levels of al-

dosterone, while hypoaldosteronism is abnormally de-

creased levels of aldosterone.

A measurement of aldosterone in blood may be termeda plasma aldosterone concentration (PAC), which may

be compared to plasma renin activity (PRA) as an

aldosterone-to-renin ratio.

5.1 Hyperaldosteronism

Primary aldosteronism, also known as primary hyperal-

dosteronism, is characterized by the overproduction of al-

dosterone by theadrenal glands,[31] when not a result of

excessive renin secretion. It leads to arterial hyperten-

sion(high blood pressure) associated with hypokalemia,

usually a diagnostic clue. Secondary hyperaldosteronism,on the other hand, is due to overactivity of therenin-

angiotensin system.

Conns syndromeis primary hyperaldosteronism caused

by an aldosterone-producing adenoma.

Depending on cause and other factors, hyperaldostero-

nism can be treated by surgery and/or medically, such as

byaldosterone antagonists.

5.2 Hypoaldosteronism

AnACTH stimulation test for aldosteronecan help in de-

termining the cause of hypoaldosteronism, with a low al-

dosterone response indicating a primary hypoaldostero-

nism of the adrenals, while a large response indicating a

secondary hypoaldosteronism.

6 Additional images

Corticosteroid biosynthetic pathway in rat

Corticosterone

7 See also

Mineralocorticoid

8 References

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[2] Hu C,Rusin CG, Tan Z,GuagliardoNA, Barrett PQ (June2012). Zona glomerulosa cells of the mouse adrenal

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22546854.

[3] Williams JS, Williams GH (June 2003). 50th anniver-

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(6): 236472. doi:10.1210/jc.2003-030490. PMID

12788829.

[4] Farrell G (May 1960). Adrenoglomerulotropin. Circu-

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[5] Hurwitz S, Cohen RJ, Williams GH (April 2004).

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[6] Palmer, LG; Frindt, G (2000). Aldosterone and potas-

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[7] Rector, Floyd C.; Brenner, Barry M. (2004). Brenner

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[8] Sherwood, Lauralee (2001). Human physiology: from

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0-534-56826-2.OCLC 43702042.

[9] Fischer AK, von Rosenstiel P, Fuchs E, Goula D, Almeida

OF, Czh B (August 2002). The prototypic miner-

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[10] Page 866-867 (Integration of Salt and Water Balance) and

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(2003). Medical Physiology: A Cellular And Molecular

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[11] Williams GH, Dluhy RG (November 1972). Aldosterone

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[12] Pratt JH (September 1982). Role of angiotensin II

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[13] Messerli FH, Nowaczynski W, Honda M,et al. (February

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[14] Felizola SJA, Maekawa T, Nakamura Y, Satoh F, Ono

Y, Kikuchi K, Aritomi S, Ikeda K, Yoshimura M, Tojo

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9 External links

Aldosterone atLab Tests Online
http://labtestsonline.org/understanding/analytes/aldosterone/tab/testhttps://www.ncbi.nlm.nih.gov/pubmed/13299331https://en.wikipedia.org/wiki/PubMed_Identifierhttps://www.ncbi.nlm.nih.gov/pubmed/5054456https://en.wikipedia.org/wiki/PubMed_Identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC292351https://en.wikipedia.org/wiki/PubMed_Centralhttps://dx.doi.org/10.1172%252FJCI107001https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC292351https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292351https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292351https://www.ncbi.nlm.nih.gov/pubmed/3971930https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1210%252Fendo-116-4-1621https://dx.doi.org/10.1210%252Fendo-116-4-1621https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pubmed/14934025https://en.wikipedia.org/wiki/PubMed_Identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1802239https://en.wikipedia.org/wiki/PubMed_Centralhttps://dx.doi.org/10.1097%252F00000658-195208000-00013https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1802239https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1802239https://www.ncbi.nlm.nih.gov/pubmed/13449153https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1210%252Fjcem-17-8-1005https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pubmed/13375573https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1210%252Fendo-59-5-526https://dx.doi.org/10.1210%252Fendo-59-5-526https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.worldcat.org/oclc/186705https://en.wikipedia.org/wiki/OCLChttps://en.wikipedia.org/wiki/Special:BookSources/0-08-013368-1https://en.wikipedia.org/wiki/International_Standard_Book_Numberhttps://www.ncbi.nlm.nih.gov/pubmed/13590935https://en.wikipedia.org/wiki/PubMed_Identifierhttp://physrev.physiology.org/cgi/pmidlookup?view=long&pmid=13590935http://physrev.physiology.org/cgi/pmidlookup?view=long&pmid=13590935https://www.ncbi.nlm.nih.gov/pubmed/4336939https://en.wikipedia.org/wiki/PubMed_Identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC292278https://en.wikipedia.org/wiki/PubMed_Centralhttps://dx.doi.org/10.1172%252FJCI106937https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC292278https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292278https://www.ncbi.nlm.nih.gov/pmc/articles/PMC292278https://www.ncbi.nlm.nih.gov/pubmed/13896654https://en.wikipedia.org/wiki/PubMed_Identifierhttp://ajplegacy.physiology.org/cgi/pmidlookup?view=long&pmid=13896654http://ajplegacy.physiology.org/cgi/pmidlookup?view=long&pmid=13896654https://www.ncbi.nlm.nih.gov/pubmed/222934https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1038%252Fki.1979.79https://en.wikipedia.org/wiki/Digital_object_identifierhttps://www.ncbi.nlm.nih.gov/pubmed/513492https://en.wikipedia.org/wiki/PubMed_Identifierhttps://dx.doi.org/10.1038%252Fki.1979.37https://en.wikipedia.org/wiki/Digital_object_identifier


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