Dr. Amel Eassawi
At the end of this lecture the student should be able to
 Enumerate the adrenocortical hormones.
 Describe the chemical nature, source and actions of
mineralocorticoid hormone.
 Describe the chemical nature, source and actions of
Glucocorticoid hormone.
 Describe the chemical nature, source and actions of
adrenal androgens hormone.
 Describe the feed back control of adrenocortical hormones.
 Describe the pathophysiology of hypo & hyper secretion of
hormones.
• Each adrenal is composed of two endocrine
organs, one surrounding the other.
• The outer layers composing the adrenal
cortex secrete a variety of steroid hormones.
• The inner portion, the adrenal medulla,
secretes catecholamines.
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• The adrenal cortex consists of three layers or
zones:
1. The zona glomerulosa, the outermost layer.
2. The zona fasciculata, the middle and largest
portion.
3. The zona reticularis, the innermost zone.
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1. Mineralocorticoids, mainly aldosterone, influence
mineral (electrolyte) balance, specifically Na+ and K+
balance.
2. Glucocorticoids, primarily cortisol, play a major role
in glucose metabolism as well as in protein and lipid
metabolism and in adaptation to stress.
3. Sex hormones are identical or similar to those
produced by the gonads (testes in males, ovaries in
females). The most abundant and physiologically
important of the adrenocortical sex hormones is
dehydroepiandrosterone, an androgen, or “male” sex
hormone.
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• Aldosterone is produced exclusively in the
zona glomerulosa.
• Cortisol synthesis is limited to the two inner
layers of the cortex, with the zona fasciculata
being the major source of this glucocorticoid
Carried in the blood extensively bound to
plasma proteins.
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• Cortisol is bound mostly to a plasma protein specific
for it called corticosteroid-binding globulin
(transcortin),
• Aldosterone and dehydroepiandrosterone are largely
bound to albumin.
• Each of the adrenocortical steroid hormones binds with
a receptor specific for it within the cytoplasm of the
hormone’s target cells
1. Mineralocorticoids bind to the mineralocorticoid
receptor (MR),
2. glucocorticoids to the glucocorticoid receptor (GR), and
3. dehydroepiandrosterone to the androgen receptor (AR).
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• The principal site of aldosterone action is on
the distal and collecting tubules of the kidney
• Promotes Na+ retention and enhances K +
elimination during the urine formation
• induces osmotic retention of H2O
• Expanding the ECF volume
• Long-term regulation of blood pressure
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• Without aldosterone, a person rapidly dies
from circulatory shock because of the marked
fall in plasma volume caused by excessive
losses of H2O-holding Na+.
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• Aldosterone secretion is increased by
1. activation of the renin-angiotensin-aldosterone
system (RAAS) by factors related to a reduction in
Na+ and a fall in blood pressure.
2. direct stimulation of the adrenal cortex by a rise
in plasma K+ concentration.
• The regulation of aldosterone secretion is
largely independent of anterior pituitary
control.
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• Cortisol, the primary glucocorticoid, plays an
important role in carbohydrate, protein, and
fat metabolism; executes significant
permissive actions for other hormonal
activities; and helps people resist stress.
• Metabolic effects The overall effect of
cortisol’s metabolic actions is to increase the
concentration of blood glucose at the expense
of protein and fat stores.
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• Hepatic gluconeogenesis
• It inhibits glucose uptake and use by many tissues, but
not the brain – increases blood glucose
• Protein degradation in many tissues, especially muscle
- increases the blood amino acid concentration
• Facilitates lipolysis – increase free fatty acids into the
blood
• Permissiveness: Cortisol must be present in adequate
amounts to permit the catecholamines to induce
vasoconstriction.
• Adaptation to stress
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• Cortisol interferes with almost every step of
inflammation.
– Blocks production of inflammatory chemical
mediators, such as prostaglandins and leukotrienes
– Suppresses migration of neutrophils
– inhibits proliferation of fibroblasts in wound repair
– interfere with antibody production by lymphocytes.
• Cortisol in turn has a profound dampening
(turning-down) impact on the immune system.
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The negative-feedback system for
cortisol maintains the level of
cortisol secretion relatively constant
around the set point.
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• Plasma cortisol concentration displays a
characteristic diurnal rhythm, with the highest level
occurring in the morning and the lowest level at
night
• Dramatic increases in cortisol secretion, mediated by
the central nervous system through enhanced
activity of the CRH - ACTH - cortisol system, occur in
response to all kinds of stressful situations.
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• Under normal circumstances, the adrenal androgens
and estrogens are not sufficiently abundant or
powerful to induce masculinizing or feminizing effects,
respectively.
• Dehydroepiandrosterone (DHEA) – a weak androgen
• This adrenal androgen governs androgen-dependent
processes in the female such as
– growth of pubic and axillary (armpit) hair,
– enhancement of the pubertal growth spurt, and
– development and maintenance of the female sex drive.
• ACTH controls the secretion of adrenal androgen but
the feed back is outside hypothalamus – pituitary adrenal axis.
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• Adrenal Medulla is a specialized ganglion of
sympathetic autonomic nervous system.
• Adrenal Medulla consists of modified
postganglionic sympathetic neurons called
CHROMAFFIN CELLS, because of their staining
preference for chromium ions.
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• Preganglionic fibers synapse directly on
Chromaffin cells in the adrenal medulla.
• The Chromaffin cells secrete hormone into the
circulation directly
- Epinephrine – 80%
- Norepinephrine – 20%
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Central
nervous system
Peripheral nervous system
Effector organs
Acetylcholine
Somatic nervous system
Skeletal muscle
Acetylcholine
Sympathetic
division
Norepinephrine
Smooth
muscle
(e.g., in
gut)
Ganglion
Epinephrine and
norepinephrine
Acetylcholine
Autonomic
nervous
system
Blood
vessel
Glands
Adrenal medulla
Acetylcholine
Parasympathetic
division
= Preganglionic axons
(sympathetic)
Cardiac
muscle
Ganglion
= Postganglionic axons
(sympathetic)
= Myelination
= Preganglionic axons
(parasympathetic)
= Postganglionic axons
(parasympathetic)
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• Both epinephrine and Norepinephrine belong to
chemical class of CATECHOLAMINES, which are derived
from the amino acid TYROSINE.
Storage of CATECHOLAMINES in CHROMAFFIN GRANULES
• Epinephrine and Norepinephrine are synthesized in the
cytosol of adrenal medulla secretary cells and stored in
Chromaffin granules.
• Epinephrine and Norepinephrine are secreted by
exocytosis.
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Epinephrine and Norepinephrine Effect On Adrenergic
Receptors:
• Adrenergic Receptors are α1, α2, β1, and β2.
• Epinephrine has effect on alpha and beta.
more effect on β2 , therefore, more effective in
bronchial asthma and skeletal muscle [where β2
receptors are present].
Norepinephrine has effect alpha and beta, more effect on
β1.
NOTE – Epinephrine discharge from adrenal medulla
always accompanies generalized sympathetic nervous
system discharge.
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Epinephrine and Norepinephrine Effect On Adrenergic Receptors
RECEPTOR TYPE
NEUROTRANSMITTER AFFINITY
α1
Norepinephrine > Epinephrine
α2
Norepinephrine > Epinephrine
β1
Norepinephrine = Epinephrine
β2
Epinephrine
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• Adrenomedullary hormones are not essential
for life, but they are very important and work
in stress response, regulation of blood
pressure and have metabolic effects.
• Sympathetic ANS and epinephrine work for
fight or flight response that is to combat
enemy or flee from danger.
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METABOLIC EFFECTS OF EPINEPRINE
Effect on Carbohydrate
1. Epinephrine mobilizes stored carbohydrates
to provide energy for use of muscular work.
2. Epinephrine increases blood glucose level by
stimulating both hepatic [liver]
Gluconeogenesis and glycogenolysis.
3. Epinephrine also stimulates glycogenolysis in
skeletal muscle.
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4. Epinephrine increases blood glucose by
inhibiting the secretion of insulin and
stimulating glucagon.
5. Epinephrine causes lipolysis, therefore,
increase blood fatty acids.
Therefore, epinephrine metabolic effect are
appropriate for fight or flight reaction.
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OTHER EFFECTS OF EPINEPHRINE
• Epinephrine affects CNS alertness – it allows
quick thinking, therefore, helps in emergency
situations.
• CNS stimulant or sedative drugs – work by
increasing or decreasing catecholamine in CNS.
• Both Epinephrine and Norepinephrine cause
sweating.
• Epinephrine dilates pupil.
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CONTROL OF EPINEPHRINE RELEASED BY
ADRENAL MEDULLA
• Catecholamine secretion from adrenal
medulla is controlled by sympathetic input to
adrenal medulla by preganglionic fibers
coming from thoracic T5-T9 and T10-T11.
• Preganglionic fibers release acetylcholine.
• Adrenal medulla release Epinephrine and
Norepinephrine into the circulation directly.
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 Human physiology, Lauralee Sherwood, seventh
edition.
 Text book physiology by Guyton &Hall,11th
edition.
 Text book of physiology by Linda .S .Costanzo third
edition
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