Adrenal gland

The adrenal glands (also known as suprarenal glands) are

Adrenal gland
endocrine glands that produce a variety of hormones including
adrenaline and the steroids aldosterone and cortisol.[1][2] They
are found above the kidneys. Each gland has an outer cortex
which produces steroid hormones and an inner medulla. The
adrenal cortex itself is divided into three main zones: the zona
glomerulosa, the zona fasciculata and the zona reticularis.[3]

The adrenal cortex produces three main types of steroid

hormones: mineralocorticoids, glucocorticoids, and androgens.
Mineralocorticoids (such as aldosterone) produced in the zona
glomerulosa help in the regulation of blood pressure and
electrolyte balance. The glucocorticoids cortisol and cortisone
are synthesized in the zona fasciculata; their functions include
the regulation of metabolism and immune system suppression.
The adrenal glands lie above the
The innermost layer of the cortex, the zona reticularis, produces
kidneys.
androgens that are converted to fully functional sex hormones
in the gonads and other target organs.[4] The production of
steroid hormones is called steroidogenesis, and involves a
number of reactions and processes that take place in cortical
cells.[5] The medulla produces the catecholamines, which
function to produce a rapid response throughout the body in
stress situations.[4]

A number of endocrine diseases involve dysfunctions of the

adrenal gland. Overproduction of cortisol leads to Cushing's
syndrome, whereas insufficient production is associated with
Addison's disease. Congenital adrenal hyperplasia is a genetic
disease produced by dysregulation of endocrine control
Endocrine system
mechanisms.[4][6] A variety of tumors can arise from adrenal
tissue and are commonly found in medical imaging when Details
searching for other diseases.[7] Precursor Mesoderm and neural crest
System Endocrine system
Artery Superior, middle and
Contents inferior suprarenal arteries
Structure Vein Suprarenal veins
Adrenal cortex Nerve Celiac and renal plexus
Medulla
Lymph Lumbar lymph nodes
Blood supply
Identifiers
Variability
Latin Glandula suprarenalis
Function
Corticosteroids MeSH D000311 (https://meshb.nl
Androgens m.nih.gov/record/ui?ui=D00
 Catecholamines 0311)

Gene and protein expression TA98 A11.5.00.001 (http://www.u

nifr.ch/ifaa/Public/EntryPag
Development
Cortex e/TA98%20Tree/Entity%20
Medulla TA98%20EN/11.5.00.001%
20Entity%20TA98%20EN.ht
Clinical significance m)
Corticosteroid overproduction
TA2 3874 (https://ta2viewer.ope
Adrenal insufficiency
nanatomy.org/?id=3874)
Adrenal tumors
FMA 9604 (https://bioportal.bioo
History
ntology.org/ontologies/FM
See also A/?p=classes&conceptid=ht
References tp%3A%2F%2Fpurl.org%2
External links Fsig%2Font%2Ffma%2Ffm
a9604)
Anatomical terminology
Structure
The adrenal glands are located on both sides of the body in the
retroperitoneum, above and slightly medial to the kidneys. In
humans, the right adrenal gland is pyramidal in shape, whereas the
left is semilunar or crescent shaped and somewhat larger.[8] The
adrenal glands measure approximately 5 cm in length, 3 cm in
width, and up to 1 cm in thickness.[9] Their combined weight in an Adrenal glands, anterior (left) and
adult human ranges from 7 to 10 grams.[10] The glands are posterior (right) surface.
yellowish in colour.[8]

The adrenal glands are surrounded by a fatty capsule and lie within the renal fascia, which also surrounds
the kidneys. A weak septum (wall) of connective tissue separates the glands from the kidneys.[11] The
adrenal glands are directly below the diaphragm, and are attached to the crura of the diaphragm by the renal
fascia.[11]

Each adrenal gland has two distinct parts, each with a unique function, the outer adrenal cortex and the
inner medulla, both of which produce hormones.[12]

Adrenal cortex

The adrenal cortex is the outer region and also the largest part of an adrenal gland. It is divided into three
separate zones: zona glomerulosa, zona fasciculata and zona reticularis. Each zone is responsible for
producing specific hormones.
The adrenal cortex is the outermost layer of the adrenal gland. Within the
cortex are three layers, called "zones". When viewed under a microscope each layer has a distinct
appearance, and each has a different function.[13] The adrenal cortex is devoted to production of hormones,
namely aldosterone, cortisol, and androgens.[14]

Zona glomerulosa
The outermost zone of the adrenal cortex is the zona glomerulosa.
It lies immediately under the fibrous capsule of the gland. Cells in
this layer form oval groups, separated by thin strands of connective
tissue from the fibrous capsule of the gland and carry wide
capillaries.[15]

This layer is the main site for production of aldosterone, a

mineralocorticoid, by the action of the enzyme aldosterone
synthase.[16][17] Aldosterone plays an important role in the long-
term regulation of blood pressure.[18] Section of human adrenal gland
under the microscope, showing its
different layers. From the surface to
Zona fasciculata
the center: zona glomerulosa, zona
fasciculata, zona reticularis, medulla.
The zona fasciculata is situated between the zona glomerulosa and
In the medulla, the central
zona reticularis. Cells in this layer are responsible for producing
adrenomedullary vein is visible.
glucocorticoids such as cortisol.[19] It is the largest of the three
layers, accounting for nearly 80% of the volume of the cortex.[3] In
the zona fasciculata, cells are arranged in columns radially oriented towards the medulla. Cells contain
numerous lipid droplets, abundant mitochondria and a complex smooth endoplasmic reticulum.[15]

Zona reticularis

The innermost cortical layer, the zona reticularis, lies directly adjacent to the medulla. It produces
androgens, mainly dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (the
precursor to testosterone) in humans.[19] Its small cells form irregular cords and clusters, separated by
capillaries and connective tissue. The cells contain relatively small quantities of cytoplasm and lipid
droplets, and sometimes display brown lipofuscin pigment.[15]

Medulla

The adrenal medulla is at the centre of each adrenal gland, and is surrounded by the adrenal cortex. The
chromaffin cells of the medulla are the body's main source of the catecholamines, such as adrenaline and
noradrenaline, released by the medulla. Approximately 20% noradrenaline (norepinephrine) and 80%
adrenaline (epinephrine) are secreted here.[19]

The adrenal medulla is driven by the sympathetic nervous system via preganglionic fibers originating in the
thoracic spinal cord, from vertebrae T5–T11.[20] Because it is innervated by preganglionic nerve fibers, the
adrenal medulla can be considered as a specialized sympathetic ganglion.[20] Unlike other sympathetic
ganglia, however, the adrenal medulla lacks distinct synapses and releases its secretions directly into the
blood.

Blood supply

The adrenal glands have one of the greatest blood supply rates per gram of tissue of any organ: up to 60
small arteries may enter each gland.[21] Three arteries usually supply each adrenal gland:[8]

The superior suprarenal artery, a branch of the inferior phrenic artery

The middle suprarenal artery, a direct branch of the abdominal aorta
The inferior suprarenal artery, a branch of the renal artery
These blood vessels supply a network of small arteries within the capsule of the adrenal glands. Thin
strands of the capsule enter the glands, carrying blood to them.[8]

Venous blood is drained from the glands by the suprarenal veins, usually one for each gland:[8]

The right suprarenal vein drains into the inferior vena cava
The left suprarenal vein drains into the left renal vein or the left inferior phrenic vein.

The central adrenomedullary vein, in the adrenal medulla, is an unusual type of blood vessel. Its structure is
different from the other veins in that the smooth muscle in its tunica media (the middle layer of the vessel) is
arranged in conspicuous, longitudinally oriented bundles.[3]

Variability

The adrenal glands may not develop at all, or may be fused in the midline behind the aorta.[12] These are
associated with other congenital abnormalities, such as failure of the kidneys to develop, or fused
kidneys.[12] The gland may develop with a partial or complete absence of the cortex, or may develop in an
unusual location.[12]

Function

Different hormones are produced in different zones of the cortex and medulla of the gland. Light
microscopy at magnification × 204.[22]

The adrenal gland secretes a number of different hormones which are metabolised by enzymes either within
the gland or in other parts of the body. These hormones are involved in a number of essential biological
functions.[23]

Corticosteroids

Corticosteroids are a group of steroid hormones produced from the cortex of the adrenal gland, from which
they are named.[24]

Mineralocorticoids such as aldosterone regulate salt ("mineral") balance and blood

pressure[25]
Glucocorticoids such as cortisol influence metabolism rates of proteins, fats and sugars
("glucose").[26]
Androgens such as dehydroepiandrosterone.

Mineralocorticoids
The adrenal gland produces aldosterone, a mineralocorticoid, which is important in the regulation of salt
("mineral") balance and blood volume. In the kidneys, aldosterone acts on the distal convoluted tubules and
the collecting ducts by increasing the reabsorption of sodium and the excretion of both potassium and
hydrogen ions.[18] Aldosterone is responsible for the reabsorption of about 2% of filtered glomerular
filtrate.[27] Sodium retention is also a response of the distal colon and sweat glands to aldosterone receptor
stimulation. Angiotensin II and extracellular potassium are the two main regulators of aldosterone
production.[19] The amount of sodium present in the body affects the extracellular volume, which in turn
influences blood pressure. Therefore, the effects of aldosterone in sodium retention are important for the
regulation of blood pressure.[28]

Glucocorticoids

Cortisol is the main glucocorticoid in humans. In species that do not create cortisol, this role is played by
corticosterone instead. Glucocorticoids have many effects on metabolism. As their name suggests, they
increase the circulating level of glucose. This is the result of an increase in the mobilization of amino acids
from protein and the stimulation of synthesis of glucose from these amino acids in the liver. In addition,
they increase the levels of free fatty acids, which cells can use as an alternative to glucose to obtain energy.
Glucocorticoids also have effects unrelated to the regulation of blood sugar levels, including the
suppression of the immune system and a potent anti-inflammatory effect. Cortisol reduces the capacity of
osteoblasts to produce new bone tissue and decreases the absorption of calcium in the gastrointestinal
tract.[28]

The adrenal gland secretes a basal level of cortisol but can also produce bursts of the hormone in response
to adrenocorticotropic hormone (ACTH) from the anterior pituitary. Cortisol is not evenly released during
the day – its concentrations in the blood are highest in the early morning and lowest in the evening as a
result of the circadian rhythm of ACTH secretion.[28] Cortisone is an inactive product of the action of the
enzyme 11β-HSD on cortisol. The reaction catalyzed by 11β-HSD is reversible, which means that it can
turn administered cortisone into cortisol, the biologically active hormone.[28]

Formation

All corticosteroid hormones share cholesterol as a common

precursor. Therefore, the first step in steroidogenesis is cholesterol
uptake or synthesis. Cells that produce steroid hormones can
acquire cholesterol through two paths. The main source is through
dietary cholesterol transported via the blood as cholesterol esters
within low density lipoproteins (LDL). LDL enters the cells
through receptor-mediated endocytosis. The other source of
cholesterol is synthesis in the cell's endoplasmic reticulum.
Synthesis can compensate when LDL levels are abnormally low.[4]
In the lysosome, cholesterol esters are converted to free cholesterol,
Steroidogenesis in the adrenal
which is then used for steroidogenesis or stored in the cell.[29]
glands – different steps occur in
The initial part of conversion of cholesterol into steroid hormones different layers of the gland
involves a number of enzymes of the cytochrome P450 family that
are located in the inner membrane of mitochondria. Transport of
cholesterol from the outer to the inner membrane is facilitated by steroidogenic acute regulatory protein and
is the rate-limiting step of steroid synthesis.[29]

The layers of the adrenal gland differ by function, with each layer having distinct enzymes that produce
different hormones from a common precursor.[4] The first enzymatic step in the production of all steroid
hormones is cleavage of the cholesterol side chain, a reaction that forms pregnenolone as a product and is
catalyzed by the enzyme P450scc, also known as cholesterol desmolase. After the production of
pregnenolone, specific enzymes of each cortical layer further modify it. Enzymes involved in this process
include both mitochondrial and microsomal P450s and hydroxysteroid dehydrogenases. Usually a number
of intermediate steps in which pregnenolone is modified several times are required to form the functional
hormones.[5] Enzymes that catalyze reactions in these metabolic pathways are involved in a number of
endocrine diseases. For example, the most common form of congenital adrenal hyperplasia develops as a
result of deficiency of 21-hydroxylase, an enzyme involved in an intermediate step of cortisol
production.[30]

Regulation

Glucocorticoids are under the regulatory influence of the

hypothalamus-pituitary-adrenal (HPA) axis. Glucocorticoid
synthesis is stimulated by adrenocorticotropic hormone (ACTH), a
hormone released into the bloodstream by the anterior pituitary. In
turn, production of ACTH is stimulated by the presence of
corticotropin-releasing hormone (CRH), which is released by
neurons of the hypothalamus. ACTH acts on the adrenal cells first
by increasing the levels of StAR within the cells, and then of all
steroidogenic P450 enzymes. The HPA axis is an example of a
negative feedback system, in which cortisol itself acts as a direct
inhibitor of both CRH and ACTH synthesis. The HPA axis also
interacts with the immune system through increased secretion of
ACTH at the presence of certain molecules of the inflammatory
response.[4] Negative feedback in the HPA axis

Mineralocorticoid secretion is regulated mainly by the renin–

angiotensin–aldosterone system (RAAS), the concentration of potassium, and to a lesser extent the
concentration of ACTH.[4] Sensors of blood pressure in the juxtaglomerular apparatus of the kidneys
release the enzyme renin into the blood, which starts a cascade of reactions that lead to formation of
angiotensin II. Angiotensin receptors in cells of the zona glomerulosa recognize the substance, and upon
binding they stimulate the release of aldosterone.[31]

Androgens

Cells in zona reticularis of the adrenal glands produce male sex hormones, or androgens, the most important
of which is DHEA. In general, these hormones do not have an overall effect in the male body, and are
converted to more potent androgens such as testosterone and DHT or to estrogens (female sex hormones)
in the gonads, acting in this way as a metabolic intermediate.[32]

Catecholamines

Primarily referred to in the United States as epinephrine and norepinephrine, adrenaline and noradrenaline
are catecholamines, water-soluble compounds that have a structure made of a catechol group and an amine
group. The adrenal glands are responsible for most of the adrenaline that circulates in the body, but only for
a small amount of circulating noradrenaline.[23] These hormones are released by the adrenal medulla,
which contains a dense network of blood vessels. Adrenaline and noradrenaline act by interacting with
adrenoreceptors throughout the body, with effects that include an increase in blood pressure and heart
rate.[23] Actions of adrenaline and noradrenaline are responsible for the fight or flight response,
characterised by a quickening of breathing and heart rate, an increase in blood pressure, and constriction of
blood vessels in many parts of the body.[33]

Formation

Catecholamines are produced in chromaffin cells in the medulla of the adrenal gland, from tyrosine, a non-
essential amino acid derived from food or produced from phenylalanine in the liver. The enzyme tyrosine
hydroxylase converts tyrosine to L-DOPA in the first step of catecholamine synthesis. L-DOPA is then
converted to dopamine before it can be turned into noradrenaline. In the cytosol, noradrenaline is converted
to epinephrine by the enzyme phenylethanolamine N-methyltransferase (PNMT) and stored in granules.
Glucocorticoids produced in the adrenal cortex stimulate the synthesis of catecholamines by increasing the
levels of tyrosine hydroxylase and PNMT.[4][13]

Catecholamine release is stimulated by the activation of the sympathetic nervous system. Splanchnic nerves
of the sympathetic nervous system innervate the medulla of the adrenal gland. When activated, it evokes the
release of catecholamines from the storage granules by stimulating the opening of calcium channels in the
cell membrane.[34]

Gene and protein expression

The  human genome  includes approximately 20,000 protein coding genes and 70% of these  genes are
expressed in the normal adult adrenal glands.[35][36] Only some 250 genes are more specifically expressed
in the adrenal glands compared to other organs and tissues.  The adrenal-gland-specific genes with the
highest level of expression include members of the cytochrome P450 superfamily of enzymes.
Corresponding proteins are expressed in the different compartments of the adrenal gland, such as
CYP11A1, HSD3B2 and FDX1 involved in steroid hormone synthesis and expressed in cortical cell
layers, and PNMT and DBH involved in noradrenaline and adrenaline synthesis and expressed in the
medulla.[37]

Development
The adrenal glands are composed of two heterogenous types of tissue. In the center is the adrenal medulla,
which produces adrenaline and noradrenaline and releases them into the bloodstream, as part of the
sympathetic nervous system. Surrounding the medulla is the cortex, which produces a variety of steroid
hormones. These tissues come from different embryological precursors and have distinct prenatal
development paths. The cortex of the adrenal gland is derived from mesoderm, whereas the medulla is
derived from the neural crest, which is of ectodermal origin.[12]

The adrenal glands in a newborn baby are much larger as a proportion of the body size than in an adult.[38]
For example, at age three months the glands are four times the size of the kidneys. The size of the glands
decreases relatively after birth, mainly because of shrinkage of the cortex. The cortex, which almost
completely disappears by age 1, develops again from age 4–5. The glands weigh about 1 g at birth[12] and
develop to an adult weight of about 4 grams each.[28] In a fetus the glands are first detectable after the sixth
week of development.[12]

Cortex
Adrenal cortex tissue is derived from the intermediate mesoderm. It first appears 33 days after fertilisation,
shows steroid hormone production capabilities by the eighth week and undergoes rapid growth during the
first trimester of pregnancy. The fetal adrenal cortex is different from its adult counterpart, as it is composed
of two distinct zones: the inner "fetal" zone, which carries most of the hormone-producing activity, and the
outer "definitive" zone, which is in a proliferative phase. The fetal zone produces large amounts of adrenal
androgens (male sex hormones) that are used by the placenta for estrogen biosynthesis.[39] Cortical
development of the adrenal gland is regulated mostly by ACTH, a hormone produced by the pituitary gland
that stimulates cortisol synthesis.[40] During midgestation, the fetal zone occupies most of the cortical
volume and produces 100–200  mg/day of DHEA-S, an androgen and precursor of both androgens and
estrogens (female sex hormones).[41] Adrenal hormones, especially glucocorticoids such as cortisol, are
essential for prenatal development of organs, particularly for the maturation of the lungs. The adrenal gland
decreases in size after birth because of the rapid disappearance of the fetal zone, with a corresponding
decrease in androgen secretion.[39]

Adrenarche

During early childhood androgen synthesis and secretion remain low, but several years before puberty
(from 6–8 years of age) changes occur in both anatomical and functional aspects of cortical androgen
production that lead to increased secretion of the steroids DHEA and DHEA-S. These changes are part of a
process called adrenarche, which has only been described in humans and some other primates. Adrenarche
is independent of ACTH or gonadotropins and correlates with a progressive thickening of the zona
reticularis layer of the cortex. Functionally, adrenarche provides a source of androgens for the development
of axillary and pubic hair before the beginning of puberty.[42][43]

Medulla

The adrenal medulla is derived from neural crest cells, which come from the ectoderm layer of the embryo.
These cells migrate from their initial position and aggregate in the vicinity of the dorsal aorta, a primitive
blood vessel, which activates the differentiation of these cells through the release of proteins known as
BMPs. These cells then undergo a second migration from the dorsal aorta to form the adrenal medulla and
other organs of the sympathetic nervous system.[44] Cells of the adrenal medulla are called chromaffin cells
because they contain granules that stain with chromium salts, a characteristic not present in all sympathetic
organs. Glucocorticoids produced in the adrenal cortex were once thought to be responsible for the
differentiation of chromaffin cells. More recent research suggests that BMP-4 secreted in adrenal tissue is
the main responsible for this, and that glucocorticoids only play a role in the subsequent development of the
cells.[45]

Clinical significance
The normal function of the adrenal gland may be impaired by conditions such as infections, tumors, genetic
disorders and autoimmune diseases, or as a side effect of medical therapy. These disorders affect the gland
either directly (as with infections or autoimmune diseases) or as a result of the dysregulation of hormone
production (as in some types of Cushing's syndrome) leading to an excess or insufficiency of adrenal
hormones and the related symptoms.

Corticosteroid overproduction

Cushing's syndrome
Cushing's syndrome is the manifestation of glucocorticoid excess. It can be the result of a prolonged
treatment with glucocorticoids or be caused by an underlying disease which produces alterations in the
HPA axis or the production of cortisol. Causes can be further classified into ACTH-dependent or ACTH-
independent. The most common cause of endogenous Cushing's syndrome is a pituitary adenoma which
causes an excessive production of ACTH. The disease produces a wide variety of signs and symptoms
which include obesity, diabetes, increased blood pressure, excessive body hair (hirsutism), osteoporosis,
depression, and most distinctively, stretch marks in the skin, caused by its progressive thinning.[4][6]

Primary aldosteronism

When the zona glomerulosa produces excess aldosterone, the result is primary aldosteronism. Causes for
this condition are bilateral hyperplasia (excessive tissue growth) of the glands, or aldosterone-producing
adenomas (a condition called Conn's syndrome). Primary aldosteronism produces hypertension and
electrolyte imbalance, increasing potassium depletion sodium retention.[6]

Adrenal insufficiency

Adrenal insufficiency (the deficiency of glucocorticoids) occurs in about 5 in 10,000 in the general
population.[6] Diseases classified as primary adrenal insufficiency (including Addison's disease and genetic
causes) directly affect the adrenal cortex. If a problem that affects the hypothalamic-pituitary-adrenal axis
arises outside the gland, it is a secondary adrenal insufficiency.

Addison's disease

Addison's disease refers to primary hypoadrenalism, which is a

deficiency in glucocorticoid and mineralocorticoid production by
the adrenal gland. In the Western world, Addison's disease is most
commonly an autoimmune condition, in which the body produces
antibodies against cells of the adrenal cortex. Worldwide, the
disease is more frequently caused by infection, especially from
tuberculosis. A distinctive feature of Addison's disease is
hyperpigmentation of the skin, which presents with other
nonspecific symptoms such as fatigue.[4]

A complication seen in untreated Addison's disease and other types

of primary adrenal insufficiency is the adrenal crisis, a medical
emergency in which low glucocorticoid and mineralocorticoid
levels result in hypovolemic shock and symptoms such as vomiting
and fever. An adrenal crisis can progressively lead to stupor and
coma.[4] The management of adrenal crises includes the application Characteristic skin
of hydrocortisone injections.[46] hyperpigmentation in Addison's
disease

Secondary adrenal insufficiency

In secondary adrenal insufficiency, a dysfunction of the hypothalamic-pituitary-adrenal axis leads to

decreased stimulation of the adrenal cortex. Apart from suppression of the axis by glucocorticoid therapy,
the most common cause of secondary adrenal insufficiency are tumors that affect the production of
adrenocorticotropic hormone (ACTH) by the pituitary gland.[6] This type of adrenal insufficiency usually
does not affect the production of mineralocorticoids, which are under regulation of the renin–angiotensin
system instead.[4]

Congenital adrenal hyperplasia

Congenital adrenal hyperplasia is a congenital disease in which mutations of enzymes that produce steroid
hormones result in a glucocorticoid deficiency and malfunction of the negative feedback loop of the HPA
axis. In the HPA axis, cortisol (a glucocorticoid) inhibits the release of CRH and ACTH, hormones that in
turn stimulate corticosteroid synthesis. As cortisol cannot be synthesized, these hormones are released in
high quantities and stimulate production of other adrenal steroids instead. The most common form of
congenital adrenal hyperplasia is due to 21-hydroxylase deficiency. 21-hydroxylase is necessary for
production of both mineralocorticoids and glucocorticoids, but not androgens. Therefore, ACTH
stimulation of the adrenal cortex induces the release of excessive amounts of adrenal androgens, which can
lead to the development of ambiguous genitalia and secondary sex characteristics.[30]

Adrenal tumors

Adrenal tumors are commonly found as incidentalomas,

unexpected asymptomatic tumors found during medical
imaging. They are seen in around 3.4% of CT scans,[7] and in
most cases they are benign adenomas.[48] Adrenal carcinomas
are very rare, with an incidence of 1 case per million per year.[4]

Pheochromocytomas are tumors of the adrenal medulla that arise

Incidences and prognoses of adrenal
from chromaffin cells. They can produce a variety of
tumors.[47]
nonspecific symptoms, which include headaches, sweating,
anxiety and palpitations. Common signs include hypertension
and tachycardia. Surgery, especially adrenal laparoscopy, is the
most common treatment for small pheochromocytomas.[49]

History
Bartolomeo Eustachi, an Italian anatomist, is credited with the first description of the adrenal glands in
1563–4.[50][51] However, these publications were part of the papal library and did not receive public
attention, which was first received with Caspar Bartholin the Elder's illustrations in 1611.[51]

The adrenal glands are named for their location relative to the kidneys. The term "adrenal" comes from ad-
(Latin, "near") and renes (Latin, "kidney").[52] Similarly, "suprarenal", as termed by Jean Riolan the
Younger in 1629, is derived from the Latin supra (Latin: "above") and renes (Latin: kidney). The
suprarenal nature of the glands was not truly accepted until the 19th century, as anatomists clarified the
ductless nature of the glands and their likely secretory role – prior to this, there was some debate as to
whether the glands were indeed suprarenal or part of the kidney.[51]

One of the most recognized works on the adrenal glands came in 1855 with the publication of On the
Constitutional and Local Effects of Disease of the Suprarenal Capsule, by the English physician Thomas
Addison. In his monography, Addison described what the French physician George Trousseau would later
name Addison's disease, an eponym still used today for a condition of adrenal insufficiency and its related
clinical manifestations.[53] In 1894, English physiologists George Oliver and Edward Schafer studied the
action of adrenal extracts and observed their pressor effects. In the following decades several physicians
experimented with extracts from the adrenal cortex to treat Addison's disease.[50] Edward Calvin Kendall,
Philip Hench and Tadeusz Reichstein were then awarded the 1950 Nobel Prize in Physiology or Medicine
for their discoveries on the structure and effects of the adrenal hormones.[54]

See also
Adrenopause

References
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External links
Adrenal gland at the Human Protein Atlas (https://www.proteinatlas.org/humanproteome/adr
enal+gland)
MedlinePlus Encyclopedia: 002219 (https://medlineplus.gov/ency/article/002219.htm)
Adrenal gland histology (http://www.proteinatlas.org/learn/dictionary/normal/adrenal+gland)
 Anatomy Atlases - Microscopic Anatomy, plate 15.292 (http://www.anatomyatlases.org/Micro
scopicAnatomy/Section15/Plate15292.shtml) – "Adrenal Gland"
Histology image: 14501loa (http://www.bu.edu/histology/p/14501loa.htm) – Histology
Learning System at Boston University
Anatomy photo:40:03-0105 (http://ect.downstate.edu/courseware/haonline/labs/l40/030105.
htm) at the SUNY Downstate Medical Center – "Posterior Abdominal Wall: The
Retroperitoneal Fat and Suprarenal Glands"
Adrenal Gland (https://web.archive.org/web/20040404014307/http://arbl.cvmbs.colostate.ed
u/hbooks/pathphys/endocrine/adrenal/index.html), from Colorado State University
Cross section image: pembody/body8a (https://www.meduniwien.ac.at/plastination/pembod
y/body8a-text.html)—Plastination Laboratory at the Medical University of Vienna

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