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Adrenal cortex hormones
Adrenal cortex
Glucocorticoid secretion
Aldosterone secretion
Androgen secretion
Adrenocortical hyperfunction
Adrenocortical hypofunction
Adrenal cortex
 Adrenal cortex, in fact, synthesizes dozens of different
types of steroid molecules, but only a few of them have
got biological activity. They have been classified into
3 categories:
1) Glucocorticoids.
2) Mineralocorticoids.
3) Androgens (sex hormones).
 These hormones initiate their action by combining with
specific intracellular receptors, and this complex bind to
specific regions of DNA to regulate gene expression.
The morphological zonation of the adrenal cortex,
showing the three types of cells with their
particular structural arrangement. and hormone
producing capability.
The hypothalamic
anterior
pituitary–adrenal
axis and
the fate of
cortisol following
its release.
CBG = cortisolbinding globulin.
Glucocorticoid secretion
 Glucocorticoids have
widespread metabolic effects
on carbohydrate, fat and
protein metabolism.
 Glucocorticoids are also
involved to some extent in
regulating sodium and water
homeostasis and the
inflammatory and stress
responses.
 In the liver, cortisol
 In the circulation,
stimulates gluconeogenesis,
glucocorticoids are mainly
amino acid uptake and
protein bound (∼90%), chiefly to
degradation,and ketogenesis.
CBG (cortisol-binding globulin or
transcortin).
 Lipolysis is increased in
 Plasma [CBG] is increased in
adipose tissue, and
pregnancy and with oestrogen
proteolysis and amino acid
treatment (e.g. oral contraceptives).
release promoted in muscle.
ACTH is the main stimulus to cortisol secretion.
3 factors regulate ACTH (and therefore cortisol) secretion:
• Negative feedback control.
• Stress. (e.g. major surgery, emotional stress) leads to a
sudden large increase in CRH (and ACTH) secretion.
• The diurnal rhythm
of plasma [cortisol]:
Patients with Cushing’s syndrome lose this diurnal variation.
Aldosterone secretion
 The principal physiological function of aldosterone is to
conserve Na+, mainly by facilitating Na+ reabsorption and
reciprocal K+ or H+ secretion in the distal renal tubule and
in other epithelial cells.
 Although its rate of production is less than 1% of the rate
of cortisol production, aldosterone is a major regulator of
water and electrolyte balance, as well as blood pressure.
 The renin–angiotensin system is the most important
system controlling aldosterone secretion.
The renin–angiotensin system
 Renin is released from the renal
juxtaglomerular cells (JC) in
response to hypotension, low
blood volume or sodium
depletion. Renin catalyses the
conversion of angiotensinogen
in plasma to angiotensin I.
During passage through the
lung, angiotensin-converting
enzyme (ACE) catalyses the
production of angiotensin II
from angiotensin I.
 The angiotensin II stimulates
release of aldosterone from the
adrenal glomerulosa and the
mineralocorticoid then
promotes reabsorption of
sodium in the distal tubules of
the kidney.
 The renin–angiotensin system is the most important
system controlling aldosterone secretion.
 Renin is a proteolytic enzyme produced by the
juxtaglomerular apparatus of the kidney . And released
into the circulation in response to a fall in circulating
blood volume or renal perfusion pressure, and by loss of
Na+ .
 Renin then acts on angiotensinogen (a 248 amino acid
peptide produced by the liver) in plasma to produce
angiotensin I (AI), a decapeptide which is then converted
by ACE in the lung to the octapeptide angiotensin II (AII).
AI and particularly AII stimulate aldosterone production in
the adrenal glomerulosa.
Androgen secretion
 The most potent androgen is testosterone, but the ones,
dehydroepiandrosterone (DHEA) and
dehydroepiandrosterone sulphate (DHEAS) are
converted by peripheral tissues into testosterone.
 The measurements of these androgens are important in
the investigation of hirsutism and virilism and CAH
( Congenital adrenal hyperplasia).
 The pathways for the production of the various adrenal
steroids are shown below.
Adrenocortical hyperfunction
 Cushing’s syndrome.
 This can be ACTH dependent or ACTH independent then
the condition is caused by tumours that release either
ACTH or cortisol.
 Approximately 70% of cases are due to a pituitary
adenoma secreting ACTH (this is known as Cushing’s
disease).
 Ectopic ACTH secretion (often from a small-cell carcinoma
of the bronchus or a carcinoid tumour) is the cause of
approximately 10% of the cases.
 Glucocorticoid- secreting adrenal adenoma or carcinoma
are each responsible for about 10% of the cases.
Adrenocortical hypofunction
(Addison’s disease)
 Adrenocortical insufficiency may be primary (e.g. destruction
of the gland itself by tuberculosis or autoimmune disease) or
secondary (e.g. hypothalamic or pituitary disease leading to
ACTH deficiency or after long-term steroid therapy).
 In primary adrenal failure, patients present with lethargy,
weakness, nausea and weight loss. They are typically
hypotensive, with characteristic hyperpigmentation affecting
the buccal mucosa, scars and skin creases.
 Patients with primary adrenal failure usually have deficiencies
of both glucocorticoids and mineralocorticoids. Often there is
hypoglycaemia with hyponatraemia, hyperkalaemia, raised
serum urea levels and acid–base disturbance.