Posterior pituitary gland
Presented by:
DR.SABRI
Posterior pituitary gland
It is made up of neural growth from the floor of
3rd ventricle of the brain forming posterior lobe
& the pituitary stalk
2 hormones are released from the gland these
are : antidiuretic hormone and oxytocin
Both are polypeptides containing 9 amino acids
They are structurally similar except for 2 amino
acids .
In ADH, phenylalanine and arginine replace
leucine and isoleucine in the oxytocin molecule
Synthesis and secretion
The 2 hormones are synthesized in the cell
bodies of the neurons in the supraoptic and
paraventricular nuclei of the hypothalamus
ADH mainly in the SON, and oxytocin
mainly in the PVN
They transported by axoplasmic flow down
the axons of these neurons to their endings
in the posterior lobe where they are stored
Hypothalamic Control of Posterior Pituitary
(Oxy)
(ADH)
Oxytocin and Vasopressin are manufactured in
the hypothalamus, but released in the posterior
pituitary.
Mechanism of release of the hormones
Stimulation of hypothalamic nuclei initiates
action potentials in their neurons
On reaching the nerve endings , cause
release of hormones by Ca2+ dependent
exocytosis
All are absorbed into the local blood vessels ,
from which they reach the general circulation
ADH hormone
Characteristics : Also known as vasopressin or arginine
vasopressin
Nona peptide 9aa
Half life : 18 min inactivated in the liver and
kidneys
In addition to the SON & PVN in the
hypothalamus , vasopressin secreting neurons
are also found in the suprachiasmatic nuclei
They also synthesized in the gonads and
adrenal cortex
Con
Vasopressin receptors :
V1A ,V1B and V2 receptors
All are G protein coupled receptors
V1A and V1B act through IP3 to
intracellular Ca 2+ content
V2 receptors act through G protein to
increase c-AMP level
Con
EFFECT [ ACTIONS] OF ADH :1. On the kidneys :
. ADH increase the permeability of the
collecting ducts of the kidneys , so water
enter the hypertonic interstitium of the
renal pyramids
. So that the urine become concentrated and
its volume decrease [antidiuretic effect]
Con
The overall effect is retention of water in
excess of solute , so the effective osmotic
pressure of the body fluids is
In the absence of ADH : the urine is
hypotonic to plasma , urine volume is
and there is a net water loss
As a result the osmolarity of the body
fluids rises
Mechanism of action of ADH
ADH bind to V2 receptors on the basolateral
membrane of the principle cells
Such binding lead to activation of the adenyl
cyclase enzyme result increase formation of
the c-AMP
c-AMP activate protein kinase A
The protein kinase A activate translocation
of aquaporin -2 channel from intracellular
vesicle to the apical membrane
Water moves passively through equaporin-2
channels
ADH Mechanism of Action
Receptor binds, causes vesicles to fuse and insert
aquaporins into the membrane
Con
2. On the blood vessels :
In large doses , ADH causes direct and powerful
V.C effect which both the peripheral resistance
and the ABP
Only large doses of ADH elevate the ABP ,
because the ADH act on the brain [at the area
postrema] to cause a decrease in COP
MECHANISM:
ADH binding to special receptors in the arteriolar
wall called V1A receptors , which act by
increasing the cytoplasmic Ca2+ content through
IP3 leading to smooth muscle contraction
Other functions
V1A receptor also found in the liver and the
brain
ADH causes glycogenolysis in the liver ,
and act as neurotransmitter in the brain
and spinal cord
V1B (also called V3) receptor found in the
anterior pituitary , which mediate increased
ACTH
Control of ADH secretion
1. Plasma osmolarity:. The release of ADH is controlled by a
feedback mechanism that maintain the
plasma osmolarity close to the 285
mosm/l
. Significant change in the ADH release
occur when the plasma osmolarity is
altered by as little as 1%
. These changes are mediated through
affecting certain osmoreceptors located in
the anterior hypothalamus out side the
blood brain barrier
Con
If the plasma osmotic pressure (e.g. due
to dehydration)
The osmoreceptors are stimulated and
discharge signals via the hypothalamohypophseal neural tract to the posterior
pituitary
Stimulating release of ADH , which the
water retention in the body
Thus correcting the dehydration & the
plasma osmotic pressure back to normal
level
Control of ADH release
1. in osmotic pressure of the ECF ( in plasma
osmolarity), as in dehydration which will
stimulate osmoreceptors in the hypothalamus
ADH.
Hyperosmolarity of
ECF
-ve
feedbac
k
Receptors in
hypothalam
us
More ADH
release
Thirs
t
Collecting ducts of
kidneys
Water
intake
Reabsorption of
water
Dilution of
ECF
Con
2. ECF volume:ADH secretion is increased when the ECF
volume is low , and decrease when the
ECF volume is high
This means that changes in the ECF
volume effect ADH release
This is mediated through affecting certain
stretch receptors in the low and high
pressure portions of the vascular system
Con
(A)The low pressure receptors : are
located in the atria , great veins and
pulmonary vessels
Which monitor the fullness of the vascular
system , and are the primary mediators that
effect the release of ADH
A moderatein the ECF volume stimulate
these receptors
impulses pass from
them via vagi which stimulate the
hypothalamic SON ADH release
which causes water retention that increase
the ECF volume to its normal level
Con
Hypovoleamia and hypotension lead to
formation of angiotensin II which ADH
release
ADH release on standing because the
blood pools in the legs and the low
pressure receptors monitor a in the ECF
volume
Con
(B)The high pressure receptors:
Arterial baroreceptors in the carotid sinus
and aortic arch act in a similar way as low
pressure receptors
They regulate the release of ADH only if
the changes in the ECF volume are large
enough to effect the ABP
Hemorrhage is the most potent stimulus
for ADH release, which by its V.C. effect
helps rise of the blood pressure
Control of ADH release cont.
2. blood volume ( 10%) stimulate
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 the
hypothalamus
More ADH
release
Thirs
t
Water
intake
More water reabsorption by
kidneys
Maintains ECF
volume
Con
3. Other factors :
ADH is released by pain , nausea ,
exercise , emotion and surgical stress
4. drugs :ADH released is stimulated by morphine ,
nicotine
And inhibited by alcohol
Abnormality
Diabetes insipidus:
This condition is caused by ADH deficiency or
failure to respond to ADH,
2 types neurogenic & nephrogenic DI
Neurogenic DI: caused by ADH deficiency due
to
1. Lesion in the hypothalamic tract
2. Lesions in the hypothalamo-hypophyseal tract
con
Nephrogenic DI: the collecting duct fail to
respond to ADH, 2 forms of disease have
been described
1. The gene for V2 receptor is mutated making
the receptor unresponsive
2. Defect in equaporin-2 because it is
autosomal gene is mutated
. These types dose not respond to treatment
with ADH agonist
Symptoms of DI
Polyuria: excretion of large amount of urine
(can reach 23l/day) the urine is colorless &
diluted
Polydipsia: drinking of large amount of
water as result of excessive sensation of
thirst caused by dehydration due to polyuria
Loss of water soluble vitamin in the urine
Syndrome of
inappropriate ADH [SIADH]
Hypersecretion of ADH sometimes occur in
patients having : cerebral diseases and also
occur in certain pulmonary diseases (e.g.
pneumonia & cancer of the lung)
Effect of SIADH
The main effect is excessive water retention
in the body which lead to
1. Sign of water intoxication
2. Marked in ECF volume , this result in
. Reduction in Na+ conc. & osmolarity of the
ECF
OXYTOCIN
Characteristics :Polypeptides 9aa
Secreted mainly by the paraventricular
Stored in the posterior pituitary
Its action on the target cells mediated by
increasing the intracellular Ca++ content
EFFECT & CONTROL OF RELEASE OF
OXYTOCIN
+ve feedback mechanism through neuroendocrine reflexes stimulated by:
Con
(1)milk ejection :
Act on myoepithelial cells in the breast tissue
causing ejection of milk as following
Stimulates of touch receptors around the
nipple, with suckling result in discharge of
impulses that activate the PVN & SON in
hypothalamus, this stimulate release of stored
oxytocin in the posterior pituitary
Oxytocin causes ejection of milk & the baby
sucks the milk& at the same time cause more
stimulation & therefore more release oxytocin
Con
Hypothalamic stimulation can also be
produced by other factors :
Certain emotional stimuli
Conditioned reflexes
PROLACTIN
OXYTOCIN
Con
[2] contraction of the smooth
muscles of the uterus :
Oxytocin causes contraction of the smooth
muscles of both the pregnant and nonpregnant uterus
The sensitivity of the uterine to oxytocin is
increased by estrogen and inhibited by
progesterone
Maintenance of pregnancy is largely due to
a high blood progesterone level
Con
In the late pregnancy , the blood progesterone
level is and the uterus becomes very sensitive
to normal blood level of oxytocin by the effect of
high blood estrogen level which may the
number of oxytocin receptors in the uterus
Oxytocin plays an important role in initiating the
labor , and its secretion is increased during it ,
which is essential for delivery of the baby and
expulsion of the placenta
Positive feedback loop
Oxytocin
Estrogen
Uterine Oxytocin receptor
contraction
x100
Cervix
dilation
Labor
Con
Mechanism :
Fetal head descends into the pelvis & starts to
stimulate touch receptors at the cervix of the uterus
Afferent impulses ascend to stimulate release of
oxytocin
Oxytocin causes contraction of the uterus, the fetus
descends more, his head start to dilate the uterus &
at the same time causes more stimulate of receptor
& more release of oxytocin until delivery of the fetus
Con
[3] Sperm transport in the female
genital tract :
The transport of sperms in the females
genitals tract during intercourse depends
not only on the motility of the sperms but
also on uterine contractions
During intercourse , oxytocin is released
leading to uterine contractions
These produce the sensation of orgasm in
Con
[4] in males :Function of the oxytocin in males it may
causes discharge of sperms from the
seminiferous tubules and the epididymis to
the vas deferens
Thank
s
