Posterior Pituitary or Neurohypophysis composed mainly of glial-like cells called pituicytes. The pituicytes do not secrete hormones. They act simply as a supporting structure for large numbers of terminal nerve fibers and terminal nerve endings from nerve tracts. That originate in the supraoptic and paraventricular nuclei of the hypothalamus.

1. Posterior Pituitary or
Neurohypophysis
Dr. Anand T. More
Tutor
Department of Physiology
D. Y. Patil Medical college, Kolhapur

2. Pituicytes
• Posterior Pituitary or Neurohypophysis composed mainly of glial-like cells
called pituicytes.
• The pituicytes do not secrete hormones.
• They act simply as a supporting structure for large numbers
of terminal nerve fibers and terminal nerve endings from nerve tracts.
• That originate in the supraoptic and paraventricular
nuclei of the hypothalamus.

3. Hormones From Posterior Pituitary
• Posterior Pituitary releases 2 hormones:
1. Antidiuretic Hormone (ADH)
2. Oxytocin
-These hormone are primarily synthesized in Hypothalamus.
-ADH & Oxytocin is primarily synthesized in supraoptic nucleus &
paraventricular nucleus respectively in hypothalamus
-Then these hormones are transferred through
Hypothalamichypophysial tract with the help of carrier proteins called
neurophysins

4. Hypothalamic control of the posterior pituitary

5. Antidiuretic Hormone (ADH)
• ADH is a hypothalamic hormone synthesized primarily in the cells of
the supraoptic nucleus .
• The hormone then pass through the axons bound to neurophysin II
(carrier protein) & stored in their endings in the posterior pituitary.
• From there ADH is subsequently released by nerve impulse arriving
along the hypothalamo-hypophysial tract.

6. Action of ADH
Action of ADH on Kidney
• ADH binds with receptors (V2 receptor) present on epithelial cells of
distal tubules & collecting ducts.
• It helps to increase permeability of distal tubules & collecting ducts to
water by increasing pore size through aquaporins 2.
• It increases water reabsorption & it leads to increase in osmolality of
urine

7. Action of ADH (High dose) on blood vessel
• ADH acts as vasoconstrictor.
• ADH binds with receptor (V1a receptor) present on vascular smooth
muscle.
• It leads to increase in intracellular calcium.
• Increase in intracellular calcium helps in contraction of vascular
smooth muscle.
• Because of this reason ADH is also known as vasopressin.

8. Regulation of Antidiuretic Hormone Production
Osmotic Stimuli
• Increased Extracellular Fluid Osmolarity (Hyperosmolality) Stimulates
Antidiuretic Hormone Secretion.
• When osmolarity of ECF increases in artery that supplies the
hypothalamus, the ADH neurons in the supraoptic and
paraventricular nuclei immediately transmit impulses into the
posterior pituitary to release large quantities of ADH into the
circulating blood

9. Osmotic Inhibitors
• Hypoosmolality of ECF Inhibit ADH secretion
Non-osmotic Stimuli
• Low Blood Volume and Low Blood Pressure Stimulate ADH Secretion
• Nausea & vomiting, Stress & drugs(e.g. nicotine, morphine,
barbiturates)- increases ADH release.
Non-osmotic Inhibitors
• High Blood Pressure or Increased Blood Volume decrease ADH
release
• Drugs(e.g. atropine, ethanol, phenytoin, lithium, caffeine), Carbon
Dioxide inhalation decrease ADH release

10. Applied Aspect
a) Syndrome of inappropriate ADH secretion (SIADH)
Cause: An excessive or inappropriate secretion of ADH from
I) the posterior pituitary
II) an ectopic (nonhypothalamic) sources e.g. a malignant tumor – bronchogenic
carcinoma
Characteristic features: Excessive ADH secretion causes
-water retention which leads to increase in blood volume & ECFV
-Decrease aldosterone secretion leads to increase excretion of sodium which
causes hypernatriuria & hyponatremia.
-It causes hypoosmolality
-The retained water in SIADH causes Oedema also further shift of water into
ICF

11. b) Diabetes Insipidus (DI)
Cause:
1) Central or neurogenic DI i.e. complete or partial failure of ADH secretion
2) Nephrogenic DI i.e. complete or partial failure of the collecting to
respond to ADH. This may be due to either V2 receptor unresponsiveness
or mutation of aquaporin-2
Features:
1) Decrease in renal water reabsorption by collecting ducts leads to
polyuria which stimulate thirst & increase water intake i.e. Polydipsia.
2) In Nephrogenic DI, urine output is directly proportional to the water
delivered to the collecting ducts.

12. Oxytocin
• Oxytocin is a hypothalamic hormone synthesized primarily in the cells
of the paraventricular nucleus.
• The hormone then pass through the axons bound to neurophysin I
(carrier protein)& stored in their endings in the posterior pituitary.
• Oxytocin Causes Contraction of the Pregnant Uterus.
• Oxytocin Aids in Milk Ejection by the Breasts.

13. Actions of Oxytocin
1) Milk ejection
-Oxytocin stimulates contraction of the smooth muscle cell (myoepithelium) lining
the duct of mammary gland; therefore causes milk ejection from lactating breast.
2) Stimulates contraction of the smooth muscle of the uterus (myometrium)
-The sensitivity of the myometrium to exogenous oxytocin during pregnancy
increases as pregnancy advances.
-Oxytocin plays a role in labour & has been shown to be a useful therapeutic
agent in the induction of labour .
3) In males, oxytocin receptors are found in the testis, epididymis & prostate gland.
-At the the time of ejaculation, oxytocin facilitates the transport of sperm towards
urethra by causing increased contraction of the smooth muscle of the vas deference.

14. Regulation of Oxytocin
A) Stimuli which increase oxytocin release
1) Oxytocin secretion is brought about by stimulation of cholinergic nerve
fibers.
2) Milk let-down reflex or Milk ejection reflex
-Suckling causes stimulation of the tactile receptors in the areolar region
of the breast
-It leads to activation of somatoasthetic neural pathways which transmit
signal to the paraventricular nuclei in hypothalamus
-It leads to release of oxytocin from posterior pituitary into blood stream.
-The Oxytocin is carried to the mammary gland where it causes milk
release

16. i) Oxytocin causes milk release in lactating women by contraction of
myoepithelial cells, which cover the stromal surface of the
epithelial of the alveoli, ducts & cisternae of the mammary glands.
Thus expelling their contained milk into the duct.
ii) Oxytocin secretion can be conditioned, therefore, the physical
stimulation of the nipples no longer is required. Thus lactating
women can experience milk release in response to the sight &
sound of a baby.

17. 3)Genital tract stimulation e.g. during coitus or parturition increases
oxytocin release
-Dilation of cervix causes stimulation of paraventricular nucleus in
hypothalamus which release oxytocin.
B) Factors which decreases oxytocin release
1) Emotional stress & psychic factor decreases milk let down
2) Activation of sympathetic neurons
-Release of epinephrine & nor epinephrine which leads to
excitation of adrenergic fibers to hypothalamus which decreases
oxytocin release
3) Drugs (e.g. ethanol, enkephalins)

18. Reference
• Textbook of Medical physiology – Guyton & Hall 12th Edition
• Textbook of physiology – A. K. Jain 5th Edition
• Net source

19. Thank You