PY8.

2
POSTERIOR
PITUITARY
GLAND
Dr.Gomathi Sivakumar MD.,
Senior Assistant Professor,
Dept. of Physiology,
KMC
POSTERIOR PITUITARY
GLAND
 Anterior vs Posterior Pituitary

 Chemical nature
 Synthesis, storage and release
 Transport and metabolism

 Actions of hormones
 Control of secretion
 Applied aspects
Anterior vs Posterior
Pituitary
Embryological Derivation

Posterior Pituitary – outgrowth of•

.hypothalamus, neural ectoderm

Anterior Pituitary- outgrowth of•

.roof of mouth, endoderm
 Histology

Control by Hypothalamus
Hormones released
Anterior Pituitary Posterior Pituitary
 Growth Hormone  Vasopresssin(ADH)
 TSH  Oxytocin
 ACTH
 FSH
 LH
 Prolactin
Posterior pituitary
hormones
Chemical nature of the
homones
Both hormones are polypeptides, each contains
9 amino acids.

Vasopressin: Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-
GlyNH2
Oxytocin: Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-
GlyNH2

In vasopressin, phenylalanine(3rd) and arginine

(8th)replace isoleucine and leucine of the oxytocin
molecule
Synthesis, storage and
release
 Both hormones are produced in hypothalamic nuclei:

- Supraoptic nucleus  (ADH + 1/6 oxytocin)

- Paraventricular nucleus  (Oxytocin + 1/6 ADH)

ADH and OTC are synthesized as large molecules, the

prohormones known as prepropressophysin and
,preprooxyphysin
respectively
• Both are transported slowly along the
 ‘hypothalamo-hypophyseal tract’ in combination
with carrier protein called ‘neurophysin’, to the
 nerve endings in the posterior pituitary gland
where they are stored.
Release
 Nerve impulse is transmitted from the cell body in
the hypothalamus down the axon- depolarizes
nerve terminal- influx of calcium- exocytosis of
vesicles
 Evidence to support that ADH and OTC
are synthesized in hypothalamus
 Herring bodies visualized in hypothalamus and posterior pituitary.
 After sectioning of the hypothalamo–hypophyseal tract, Herring
bodies disappear below the section and fill up proximal to the point
of section.
 Newly synthesized hormone can be released into the circulation
from the hypothalamus even in the absence of posterior pituitary
 Destruction of supraoptic/PV nucleus causes disappearance of
Herring bodies
Transport and metabolism
 Biological half-life of ADH is 16–20 min.
Oxytocin 1 – 6 min.
 Metabolism.

Rapidly inactivated in the liver and kidney.

Actions of hormones
Action of ADH
 ADH has 2 main effects:

1.  water re-absorption (retention) by distal tubules

& collecting ducts of the kidneys
* V2 receptors
cAMP.

2. Contraction of vascular smooth muscles 

generalized vasoconstriction.
* V1 receptors
IP3/Ca2+.
Control of Secretion of ADH
Control of ADH release
1. Hyperosmolality - in osmotic pressure of the ECF (
in plasma osmolality), as in dehydration which will
stimulate osmoreceptors in the hypothalamus  
ADH. Hyperosmolarity of ECF
-ve feedback

Receptors in
hypothalamus

More ADH release Thirst

Collecting ducts of kidneys  Water intake

Reabsorption of water

Dilution of ECF
Control of ADH release … cont.
2. Hypovolemia – blood volume ( 10%) 
mechanoreceptors in the great arteries (aorta & carotids) &
right atrium   ADH.
Loss of ECF volume

Less pressure in Rt.

atrium & great vessels

Less nerve impulse to Thirst

the hypothalamus

More ADH release  Water intake

More water reabsorption by kidneys

Maintains ECF volume
 Control of ADH release …cont.

3. Pain, emotional stress & physical trauma   ADH secretion.

4. Drugs, e.g. morphine, barbiturates, & nicotine   ADH

secretion.

5. Alcohol   ADH secretion.

Interaction of hypovolaemia and plasma
osmolality
 The hypovolaemia sensitizes the ADH response to
hyperosmolality.
 However, if hypovolaemia is severe (e.g. after
severe haemorrhage)
baroregulation overrides osmotic regulation
ADH secretion is stimulated, even though plasma
osmolality may be below 270 mOsm/L.
Applied Aspects
Hypo and Hypersecretion of ADH
Abnormalities of ADH release – Hyposecretion:
 Lack of ADH  Diabetes insipidus.
2 types of DI: a. Neurogenic (central, or cranial) …
Problem in Hypothalamus or Post pituitary
gland.
R/: ADH(Desmopressin)
b. Nephrogenic …resistance of V2 receptors
in collecting ducts of the kidneys? Lithium
induced
- No ADH is needed as treatment.

Symptoms: Polyuria  20 L/day (N  1.5 L/d), Polydipsia,

 specific gravity of urine (diluted urine),
 plasma osmolality.
 Abnormalities of ADH release – Hypersecretion:
  ADH SIADH
Causes
 - occurs after surgery.
- Ectopic ADH from tumours in Brain and lungs
Signs & Symptoms:
- Hyponatremia(due to Dilution of ECF and Hypernatiuria)
- Mental confusion.
- Coma.
- Death, due to ventricular fibrillation.
Treatment
Drugs like demeclocycline, which blocks effect of ADH on kidneys.
Actions of Oxytocin
Copyright © 2005 Pearson Education, Inc.,
.publishing as Benjamin Cummings
Action of oxytocin
1. Contraction of smooth muscles of the uterus 
enhance labor.
2. Contraction of mammary gland myoepithelial cells of
the alveoli & the ducts  Ejection of milk as a reflex in
lactating women.
3. In men  Contraction of vas in ejaculation.

Remember: Oxytocin is concerned with releasing or

ejection of milk, while prolactin is concerned with
synthesis & production of milk.
Control of oxytocin release
Control of oxytocin release
1. Stimulation of nipple (suckling reflex)   oxytocin.

2. Visual or auditory stimuli from the baby   oxytocin secretion.

3. Distension of uterus & stretching of cervix during delivery  

oxytocin release.

4. Hormones: a. progesterone   uterine sensitivity to oxytocin.

b. estrogen   uterine sensitivity to oxytocin.
5. Alcohol   oxytocin secretion.
6. Psychological & emotional factors, e.g. Fear, anxiety & pain  
oxytocin.
Clinical importance of
oxytocin
Syntocinon
 Induction of labour
 Control of postpartum haemorrhage
POMC
 Synthesized by Intermediate-lobe cells and
corticotropes of the anterior lobe
POMC - Products
 Incorticotropes, it is hydrolyzed to
ACTHMelanocyte stimulating activity
LPH
β-endorphin

 In the intermediate lobe cells, POMC is hydrolyzed to

corticotropin-like intermediate-lobe peptide (CLIP)
β-LPH(Lipotrophin
β-endorphin
MSH
 Abnormal pallor - hallmark of hypopituitarism.
 Hyperpigmentation occurs in patients with adrenal
insufficiency due to primary adrenal disease.
 Hyperpigmentation in association with adrenal
insufficiency rules out the possibility that the
insufficiency is secondary to pituitary.
 Albinos - genetic defects in the pathways for
melanin synthesis from dopamine.
 Piebaldism is characterized by patches of skin that
lack melanin as a result of congenital defects in the
migration of melanocyte precursors from the neural
crest during embryonic development.
 Vitiligo involves a similar patchy loss of melanin,
but after birth secondary to an autoimmune process
that targets melanocytes.
Albinism
Piebaldism
Vitiligo