The document discusses the adrenal glands and their hormones. It describes that the adrenal glands are divided into the outer cortex and inner medulla. The cortex secretes steroid hormones like cortisol and aldosterone. Cortisol regulates carbohydrate, protein, and fat metabolism. Aldosterone regulates sodium and potassium levels. The medulla secretes catecholamines like epinephrine and norepinephrine which increase heart rate and mobilize energy stores. The hormones act through complex feedback mechanisms and play important roles in the stress response.
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6.Adrenal galnds.ppt
1. Hormones of the Adrenal Glands
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2. Adrenal Glands
• Suprarenal glands
• Divided into
– outer Cortex and inner Medulla
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3. Adrenal Glands
• Suprarenal glands weigh 5 gm
• Divided into outer Cortex (80% of gland)
and inner Medulla (20% of gland)
• Despite their organization
– into a single gland, the medulla and cortex
are functionally different endocrine organs,
and have different embryological origins.
• The medulla
– is derived from ectoderm (neural crest),
– while the cortex develops from mesoderm.
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5. Adrenal Medulla
• Cells in the adrenal medulla
– synthesize and secrete catecholamine
• norepinephrine, epinephrine & dopamine
– also small amount of opioid peptides
• met-enkephalin, leu-enkephalin
• Roughly 80% of the catecholamine output
is epinephrine
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6. Adrenal Medulla
In adrenal medulla
The chromaffin cell is the principle
cell type.
There are epinephrine releasing
chromaffin cells and norepinephrine
releasing cells
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7. Adrenal Medulla
• 80% of chromaffin cells
– secrete adrenalin
– 20% secrete nor adrenalin
The medulla is richly
innervated
by preganglionic sympathetic
fibers
and is, in essence, an extension
of the sympathetic nervous
system.
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8. Adrenal Medulla
• The chromaffin cells
– are like the post
ganglionic cells
– in the sympathetic
nervous system
• The pre-ganglionic
fibres
– Originate from T5 – T9
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T5 – T9
Symp pre-
ganglionic
nerve
Chromaffin
cells
Adrenalin
Noradrenalin
9. Adrenal Medulla
• These preganglionic
fibres
– release acetylcholine
as the
neurotransmitter
• Ach cause the
chromaffin cells to
release
– Adrenalin
– Nor-adrenalin
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T5 – T9
Symp pre-
ganglionic
nerve
Chromaffin
cells
Adrenalin
Noradrenalin
Ach
10. Adrenal Medulla
• Adrenalin
– Mainly produced in adrenal medulla
– Small amount is secreted in brain
• Nor adrenalin
– Widely distributed in neural tissues
including
• Adrenal medulla
• Sympathetic postganglionic fibers
• CNS
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12. Control of Secretion
• Secretion of catecholamine
– by chromaffin cells is stimulated by
• Acetylcholine
• Angiotensin II
• Histamine
• Bradykinin
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13. Control of Secretion
• Stress
– Flight or fight reaction
– Activation of sympathetic system
• Fear, anxiety, pain, trauma,
hemorrhage
• Any stressful situation
– Lead to release of catecholamines
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14. Physiological Actions
• In general,
– circulating
epinephrine&norepinephrine
– released from the adrenal medulla
– have the same effects on target
organs as direct stimulation by
sympathetic nerves.
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15. Physiological Actions
• Complex physiologic responses
– result from adrenal medullary
stimulation
– because there are multiple
receptor types
– which are differentially expressed
– in different tissues and cells
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16. Physiological Actions
• Effects depend on the type of
receptors on target organ
– receptors or receptors
• Adrenaline act on both and
receptors
• Nor adrenaline act mainly on
receptors
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17. Physiological Actions
• Adrenergic receptors
– Associated with excitatory function of
the body
– Associated with inhibitory functions of
intestinal motility
• Adrenergic receptors
– Associated with most of inhibitory
functions of the body
• Except on the myocardium
–Excitation
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18. Physiological Actions
• Effects on the heart
–Nor-adrenalin & adrenalin both
increase the
• Heart rate, force of
contraction (1 receptors)
–Increase effectiveness of the
heart
• Myocardial excitability
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22. Hormones of the Adrenal cortex
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23. Adrenal Cortex
• Synthesize and secrete
– steroid hormones (corticosteroids)
• Synthesize from steroid
cholesterol
• Have nearly similar chemical formula
• Slight differences in molecular
structure give them different
functions
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24. Corticosteroids
• Three groups of corticosteroids
• Mineralocorticoids
– Effect on electrolytes
• Glucocorticoids
– Exhibit important effect in
increasing blood glucose
concentration
– Also affect fat, protein metabolism
• Androgens
– Sex hormones
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25. Adrenal Cortex
• Histologic
examination
– of the cortex
reveals
– three concentric
zones of cells
– that differ in the
major steroid
hormones
– they secrete
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Glomerulosa
Fasciculata
Reticularis
Medulla
27. Adrenal Cortex
• Zona fasciculata
– middle layer of
cortex
• Zona reticularis
– Innermost layer of
cortex
• Zona fasciculata &
reticularis
– Secrete cortisol &
androgens
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Glomerulosa
Fasciculata
Reticularis
Medulla
28. Structure of steroid hormones
• All steroids
– have the same
basic
cyclopentanoperh
ydrophenanthrene
ring structure
• Have
– 3 cyclohexyl rings
• ( A, B, C)
– One cyclopentyl
ring (D)
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19
3
2
1
8
7
6
5
4
10
9
15
14
13
12
11
18
17
16
A B
C D
Cyclopentanoperhydrophenanthrene
30. Transport & Fate of Adrenal
Hormones
• Cortisol
– Combine with Cortisol binding
globulin (CBG)
• Transcortin
• Also can combine with
albumin
• About 94% transported in
bound form; 6% in free form
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31. Transport & Fate of Adrenal
Hormones
• Aldosterone
–Combine loosely with plasma
protein
–About 50% is in free form
• Both combined and free forms
–are transported through out ECF
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32. Transport & Fate of Adrenal
Hormones
• Adrenal steroids degraded in liver
• Conjugated to glucoronides or
sulfated to sulfate
– Then 25% excreted though bile
– 75% excreted through urine
• Hence diseases of liver
– Greatly affect hormone degradation
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34. Functions of Glucocorticoids
• Affect metabolic systems for
utilizing
– Carbohydrates
– Proteins
– Fats
• 95% of glucocorticoid activity
– of adrenal cortex
– result from Cortisol
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35. Mechanism of Action
• Multiple effects
– of glucocorticoids
– triggered by
– binding to
intracellular
receptors
– which interact with
specific regulatory
DNA sequences
• Glucocorticoids
Response Element
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36. Mechanism of Action
• Induce or repress
– gene transcription
• Leads to increased
or decreased
– formation of mRNA
• Alters synthesis of
enzymes
• Alter cell
functions
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37. Effects of Cortisol on carbohydrate
metabolism
• Stimulate gluconeogenesis
– liver enzymes for converting
AA into glucose
• glucose utilization by cells
– Exert anti insulin effect
• Block glucose transport in muscle
& adipose tissue
• Cortisol indirectly inhibit activity of
glycolytic enzymes
• Glucokinase, phosphofructokinase,
pyruvate kinase
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38. Effects of Cortisol on Protein
Metabolism
• Glucocorticoids enhance protein
catabolism in skeletal muscle, and
other extra hepatic tissues
• Released AA are transported to
liver where are converted to glucose
• Glucocorticoids inhibit protein
synthesis
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39. Effects of Cortisol on Fat
Metabolism
• Glucocorticoids are lipolytic
– Potentiate lipolytic actions of
other hormones
• GH, catecholamines, glucagon,
T3,T4
– Favour FA mobilization
• from adipose tissue to liver
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40. Fat Metabolism
• FFA metabolized by liver
– -Oxidation
• formation of ketone bodies
– Inhibit glycolysis
• Fructose 1,6 diphosphatase
– Activated by FA
• Pyruvate kinase ,
phosphofructokinase
– Inhibited by FA
• Glycolysis is inhibited,
gluconeogenesis proceeds
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41. Fat Metabolism
• Glucocorticoids indirectly
stimulate lipolysis by
– Blocking peripheral glucose
uptake, utilization
– Inhibit re-esterification of FA in
adipose tissue
• Inhibit the use of glucose
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42. Effects of Cortisol on Fat
Metabolism
• Cortisol inhibit FA synthesis in the
liver
– This effect is not observed in adipose
tissue
• Overall effect
– Redistribution of body fat
– In total body fat
• Truncal obesity
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43. Effects of Cortisol on Fat
Metabolism
• Characteristic centripetal
distribution of fat
– Accumulation of fat on central
axis of body
– Deposition of fat on the face
• Moon face
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44. Effects of Cortisol on Fat Metabolism
• Deposition of fat in supra
scapular region
• Buffalo hump
– Excessive fat distribution
• Pendulous abdomen
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45. Anti-inflammatory and
immunosuppressive effects
• The anti-inflammatory and
immunosuppressive effects
– of glucocorticoids are largely secondary
to their inhibition of the immune responses
• of lymphocytes, macrophages, and
fibroblasts.
• Also by stabilizing the lysosomes
– of damaged cells
– preventing the release of the mediators of
inflammation
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46. anti-inflammatory and
immunosuppressive effects
• Whereas NSAIDs principally
– inhibit prostaglandin synthesis,
– corticosteroids interfere earlier
– in the inflammatory cascade
– by inhibiting PLA2 actions
– and thereby curtailing
• both the leukotriene and
prostaglandin mediated inflammatory
response
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47. anti-inflammatory and
immunosuppressive effects
• increased levels of
glucocorticoids
– serve to suppress the immune
system.
• This is achieved by decreasing
– the production of lymphocytes
(especially T cells) and antibodies
– Also reduce number of eosinophils
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48. Control of Secretion
• Hypothalamus
– under the influence of
higher centers
– Releases Corticotrophin
releasing hormone
(CRH)
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Limbic system
CRH
Hypotha
lamus
ACTH
Adeno-
hypophysis
Plasma
cortisol
conc
Adrenal
cortex
Negative
feed back
49. Control of Secretion
• CRH acts on
anterior pituitary
– Releases ACTH
• ACTH acts on
adrenal cortex (zona
fasciculata)
– Releases cortisol
– Released into plasma
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Limbic system
CRH
Hypotha
lamus
ACTH
Adeno-
hypophysis
Plasma
cortisol
conc
Adrenal
corte
Negative
feed back
50. Control of Secretion
• Conc of plasma
cortisol
– Negative feedback
inhibition
• Hypothalamus
• Anterior pituitary
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Limbic system
CRH
Hypotha
lamus
ACTH
Adeno-
hypophysis
Plasma
cortisol
conc
Adrenal
corte
Negative
feed back
54. Aldosterone
• Secreted by the cells
– of the zona glomerulosa
• Functions
–Increase Na+ re-absorption by
• the kidneys, sweat glands,
salivary glands, GIT
–Increase excretion of K+, H+
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55. Mechanism of Action
• Site of action
–Act on the
Principal cells
–of the late
distal
tubules&Cortic
al collecting
duct
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Na+
Na+
K+
Lumen
ISF
Na+
56. Mechanism of Action
• Thus Aldosterone
– Increase the
number of Na-K
ATPase molecules
in the basal lateral
membrane
• Aldosterone increase
the exchange of
sodium and
potassium
– Na+ conservation in
ECF
– K+ is excreted
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Na+
Na+
K+
Lumen
ISF
Na+
57. Control of Aldosterone Secretion
• ECF volume/Blood volume
• Arterial BP
• K+ conc in ECF leads to an
in aldosterone secretion
• Na+ conc in ECF inhibits
aldosterone secretion
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58. Atrial Natriuretic Peptide (ANP)
• ANP inhibit production of
–Renin
–Aldosterone
• Leads to a reduction of Na+ by
the nephrons and hence
–Increased Na+ excretion in urine
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