A small gland that makes steroid hormones, adrenaline, and noradrenaline. These hormones help control heart rate, blood pressure, and other important body functions. There are two adrenal glands, one on top of each kidney. Also called suprarenal gland.

1. Adrenal gland

2. Anatomy
• There are 2 adrenal glands each weighing
about 4 gms
• They lie at the superor poles of the two
kidneys
• Each gland is composed of two distinct parts
adrenal cortex and adrenal medulla
• Blood supplied by superior ,inferior and
middle adrenal arteries

3. location

4. Section of adrenal gland

5. Adrenal cortex
Three distinct layers-
• Zona glomerulosa- thin layer under the
capsule 15% of the cortex. The cells here
capable of secreting significant amount of
aldosterone (mineralcorticoid)
• Zona fasiculata- middle widest layer 75%of
cortex secreting glucocorticoids (cortisol and
corticosterone) as well as small amount of
adrenal androgens

6. Adrenal medulla
• It occupies the central 20 % of the adrenal
gland
• It secretes the hormones epinephrine and nor
epinephrine in response to sympathetic
stimulation they are referred to as
catecholamines

7. Biosynthesis of adrenal steroids
• Important steroid products of adrenal cortex are
aldosterone , cortisol and androgens
• All the steps of synthesis occur in the
mitochondria and endoplasmic reticulum
• Approx 90-95% of cortisol in plasma binds to
plasma protein globulin called transcortin and to
albumin
• Binding serves as a reservoir to lessen rapid
fluctuations in free hormone concentration
• Adrenal steroids are degraded mainly by liver and
conjugated to glucuronic acid or sulphates

9. ADRENAL CORTEX
• ZONA GLOMERULOSA- MINERALOCORTICOID-
ALDOSTERONE

10. Mineralocorticoid- aldosterone
• Aldosterone is the principal mineralocorticoid
secreted by the adrenal glands
• Aldosterone exerts 90% of the mineralocorticoid
activity of adrenal cortex rest 10 % is by cortisol
• Aldosterone increases the reabsorption of
sodium ions in the ECF
• It acts on principal cells of collecting ducts in the
kidney increasing sodium in exchange of
potassium and hydrogen ions

11. Renin angiotensin aldosterone system
(RAAS)
• Aldosterone secretion is mainly controlled by
angiotensin and potassium acting directly on
adrenocortical cells
• Angiotensinogen precursor (liver)…..renin from
kidneys (proteolytic) cleaves….angiotensin
l…..protease angiotensin converting enzyme in the
endothelial membrane….angiotensin ll
• Angiotensin ll acts on the membrane receptors of
plasma membrane in the adrenal glands and
activates IP3 to synthesise aldosterone
• Aldosterone enters circulation and act on the kidney
(stimulate Na+ & water retention, K+ & H+ excretion in

12. Factors that play a role in regulation of
aldosterone
• Increased potassium ion concentration in the
extracellular fluid
• Increased angiotensin II concentration in ECF
• Increased sodium ion concentation in ECF
• ACTH from anterior pituitary

14. Physiological functions of cortisol
• It has other non stress effects
• Has permissive actions on reactivity of
catecholamines on muscle cells around blood
vessels (blood pressure)
• Basal levels also required by enzymes of
metabolic homeostasis
• Anti-inflammatory & anti-immune functions
• Reduces capillary permeability in injured areas
• Saves as a brake on the immune system
• Important developmental hormone

15. Effect of cortisol in preventing
inflammation
• Cortisol stabilizes the lysosomal membrane
• Cortisol decreases the permeability of the
capillaries preventing loss of plasma into tissues
• Cortisol decreases migration of WBCs into
inflamed area and phagocytosis of damaged cells
• Cortisol suppresses the immune system causing
lymphocyte production to decrease
• Cortisol attenuates fever as it reduces the release
of interleukin-1

16. Effects of increased cortisol levels during stress
1. Effects on organic metabolism
a. Stimulation of protein catabolism in bone, lymph, muscle etc.
b. Stimulation of liver uptake of amino acids and their conversion
to glucose (gluconeogenesis).
c. Inhibition of glucose uptake and oxidation by many body cells
(“insulin antagonism”), but not by the brain.
d. Stimulation of triglyceride catabolism in adipose tissue, with
release of glycerol and fatty acids into the blood.
2. Enhanced vascular reactivity (increased ability to maintain vasoconstriction in
response to norepinephrine and other stimuli).
3. Unidentified protective effects against the damaging influence of stress
4. Inhibition of inflammation and specific immune responses.
5. Inhibition of nonessential functions (eg., reproduction and growth).

17. Actions of the Sympathetic Nervous system , including
epinephrine secreted during stress
1. Increased hepatic and muscle glycogenolysis (provides a quick
source of glucose).
2. Increased breakdown of adipose tissue, tissue triglyceride
(provides a supply of glycerol for gluconeogenesis and fatty acids
for oxidation).
3. Decreased fatigue of skeletal muscle.
4. Increased cardiac function (eg., increased heart rate).
5. Diverting blood from viscera to skeletal muscle by means of
vasoconstriction in the former beds and vasodilation in the
latter).
6. Increased lung ventilation by stimulating brain breathing centres
and dilating airways.

18. Other hormones released during
stress
• Aldosterone, vasopressin (ADH), growth
hormone, glucagon, and bea-endorphin
coreleased with ACTH,
• Overall effects of changes in GH, glucagon and
insulin, like those of cortisol and epinephrine,
to mobilise energy stores
• Chronic stress can have deleterious effects

20. Regulation of cortisol secretion
• ACTH stimulates cortisol secretion
– Secretion of cortisol is controlled entirely by ACTH
• ACTH activates by increase in cAMP
– ACTH acts on adrenocortical cells to activate
adenyl cyclase
– Long term activation can cause hypertrophy
• Inhibitory effect of cortisol
– Cortisol sends negative feedback to hypothalamus
and pituitary to regulate cortisol levels

21. Different types of stress that increase
cortisol release
• Trauma of any type
• Infection
• Intense heat or cold
• Injection of norepinephrine
• Surgery
• Any debilitating disease

22. Hypoadrenalism (Addison’s disease)
• This is due to insufficient adrenocortical
hormones
• Most common cause is primary atrophy or
injury, tuberculous destruction of the gland or
cancer
• Disturbances cause mineralocorticoid
deficiency, Glucocorticoid deficiency and
melanin pigmentation

23. Features of Addison’s disease

24. Addison’s disease
• Mineralocorticoid deficiency
– Results in loss of sodium ions, chloride ions and water to be lost
into urine
– This results in hyponatremia,hypercalemia and mild acidosis
– Plasma volume falls, cardiac output and blood pressure
decreases and patient dies in shock
• Glucocorticoid deficiency
– No proper synthesis of glucose, reduced mobilization of proteins
and fats
• Melanin pigmentation
– Melanin pigmentation of mucous membrane and skin
– Melanin deposited in blothes in thin areas of the skin due to
increased sectretion of MSH

25. Hyperadrenalism- Cushing’s syndrome
Hypercorticolism can occur due to-
• Adenomas of the anterior pituitary secreting
increased ACTH
• Abnormal function of hypothalamus causing
increased CRH and thereby increased ACTH
• Adenomas of the adrenal cortex
When cushing’s syndrome is secondary to excess
secretion of ACTH by the anterior pituitary this is
called Cushing’s disease

29. Tests for adrenal dysfunction