Neurohypophysis

(HIPOFISE POSTERIOR)
 Neurohypophysis

The posterior pituitary arises from the forebrain (neural

tissue) during development and lies below the
hypothalamus with which it forms a structural and
functional unit known as the neurohyopophysis

Neurohypophysis consists of 3 parts:

1. Supraoptic and paraventricular nuclei of hypothalamus
(contain cell bodies of the magnocellular neurons that
synthesize and secrete Vasopressin (ADH) and
Oxytocin)
2. Posterior hipofisis muncul dari otak depan (jaringan
saraf) selama pengembangan dan terletak di bawah
hipotalamus dengan yang membentuk unit struktural
 Neurohypophysis

2. Hypothalamic- Neurohypophyseal nerve tract (axons

of neurons)

3. Posterior pituitary (axons terminate on capillaries of

the inferior hypophyseal artery)
Hipotalamus Neurohypophyseal saluran
saraf (akson neuron)
3. Posterior hipofisis (akson berakhir
pada kapiler dari arteri hypophyseal
rendah)
Neurohypophysis
 Vasopressin and Oxytocin

The genes encoding ADH and oxytocin are on chrm 20

Synthesized as prohormones consisting of peptide
hormone + associated binding peptide or neurophysin
(functions as carrier protein)

ADH + neurophysin II
Oxytocin + neurophysin I

Transported in secretory granules via axoplasmic flow to

nerve endings of the posterior pituitary
Gen yang mengkode ADH dan oksitosin yang chrm 20
Disintesis sebagai prohormones terdiri dari hormon
peptida + terkait peptida mengikat atau neurophysin
 Vasopressin and Oxytocin

In the secretory granules the prohormone undergoes

further processing to produce mature peptide hormone +
neurophysin (equimolar amounts)

Action potentials that reach the nerve endings increase

Ca influx- hormone secretion

ADH and oxytocin circulate unbound to plasma proteins

They have a short half life (5-15min)
Dalam butiran sekresi prohormon yang mengalami
pengolahan lebih lanjut untuk menghasilkan peptida
hormon dewasa + neurophysin (jumlah molar yang
sama)
 Oxytocin

In women, oxytocin contracts the pregnant uterus and

also causes breast duct smooth muscle contraction
leading to breast-milk ejection during breast feeding

It is released in response to suckling and also to cervical

dilatation during childbirth

Oxytocin deficiency has no known adverse effects

Pada wanita, oksitosin kontrak rahim hamil dan juga
menyebabkan saluran payudara kontraksi otot polos
yang menyebabkan ASI ejeksi selama menyusui

Hal ini dirilis dalam menanggapi menyusui dan juga

 ADH/ Vasopressin

There are 3 vasopressin receptors:

V1 Location: Vascular smooth muscle (Liver, platelets,
CNS)
Action: Vasoconstriction (enhanced platelet adhesion,
glycogenolysis, neurotransmitter)

V2 Location: Basolateral membrane of distal nephron

Action: Antidiuresis via production and action of
acquaporin 2

V3 Location: Pituitary corticotroph

Action: Enhanced ACTH release (partly by enhancing
action of CRH)
Ada 3 reseptor vasopressin:
V1 Lokasi: Vascular otot polos (Liver, trombosit, CNS)
 Functions of ADH

The primary function of ADH is to regulate extracellular

fluid volume by affecting renal handling of water. Its main
action is to reduce free water clearance.
It is also a vasoconstrictor and pressor agent (hence, the
name "vasopressin").
AVP acts on renal collecting ducts via V2 receptors to
increase water permeability (cAMP-dependent
mechanism), which leads to decreased urine formation
(hence, the antidiuretic action of "antidiuretic hormone").
A secondary function of ADH is vasoconstriction. ADH
binds to V1 receptors on vascular smooth muscle to
cause vasoconstriction
Fungsi utama dari ADH adalah untuk mengatur volume
 Renal actions of ADH

The major renal effect of ADH is to increase the water

permeability of the luminal membrane of the collecting
duct epithelium via the ADH sensitive water channels
acquaporin 2 -results in concentrated urine (>osmolality)

ADH binds to V2 receptor

This results in activation of adenyl cyclase via the stimulation of G-
alpha-s heterometric proteins,
The increased levels of cAMP activate protein kinase A and the
fusion of vesicles consisting of water channel proteins (AQP2) with
the luminal membrane
ADH also stimulates urea absorption in the descending limb and the
inner medullary collecting duct via urea transporters
Efek ginjal utama ADH adalah untuk meningkatkan permeabilitas air
dari membran luminal dari duktus pengumpul epitel melalui ADH
saluran air sensitif acquaporin 2 -results dalam urin terkonsentrasi
 Stimuli for ADH secretion

Plasma osmolality (> extracellular osmolality leading to

cellular dehydration) is the most important stimulus

Plasma osmolality changes of as little as 1-2% are

detected by hypothalamic osmoreceptors. Signals are
transmitted to the supraoptic and paraventricular nuclei
where ADH is synthesized.

The relationship between plasma osmolality and ADH

concentration is linear. (Relationship lost with drinking-
suppression of ADH release)
The threshold for ADH secretion is 284.3mOsm/kg.
Urine is maximally concentrated (>800mOsm/kg) at a
plasma osmolality of 295mOsm/kg
Osmolalitas plasma (> osmolalitas ekstraseluler
menyebabkan dehidrasi seluler) adalah stimulus yang
Stimuli for ADH secretion
Stimuli for ADH secretion
 Stimuli for ADH secretion

Decreased extracellular fluid volume (without change in

osmolality) stimulates thirst and ADH secretion
(e.g.hemorrhage)
Small decreases in volume have minimal effect on ADH
levels; reductions >10% cause a marked increase in
ADH secretion. (hyperbolic relationship-not linear)
These high levels do not cause further water
conservation (max urinary concentrations are reached at
much lower levels)
The high levels of ADH probably support blood pressure
via V1 receptors
Penurunan volume cairan ekstrasel (tanpa perubahan
osmolalitas) merangsang rasa haus dan ADH sekresi
Hypovolemic stimulus to ADH release
 Stimuli for ADH secretion

Interaction of osmolality and volume

2 mechanisms involved in hypovolemic stimulation of
ADH and thirst:
1. Moderate reductions in blood volume result in
decreased stimulation of mechanoreceptors in the atria
and central veins.
Atrial receptor firing normally inhibits the release of
ADH by the posterior pituitary. With hypovolemia or
decreased central venous pressure, the decreased
firing of atrial stretch receptors leads to an increase in
ADH release.

nteraksi osmolalitas dan volume

2 mekanisme yang terlibat dalam stimulasi
 Stimuli for ADH secretion

More severe hypovolemia (hypotension <5-10mmHg)

results in decreased firing of arterial baroreceptors.
This leads to enhanced sympathetic activity, which
increases ADH release.

2. Hypovolemia stimulates renin secretion and

angiotensin formation. Angiotensin II also stimulates
thirst and ADH secretion
Lebih parah hasil hipovolemia (hipotensi <5-10mmHg)
di tembak penurunan baroreseptor arteri. Hal ini
menyebabkan aktivitas simpatik ditingkatkan, yang
meningkatkan pelepasan ADH.
 Stimuli for ADH secretion

Regulation of water balance involves interaction

between osmotic and volume stimuli
For a given increase in osmolality, the increase in
plasma ADH will be greater in hypovolemic than in
normovolemic states

Other factors known to increase ADH levels include

nausea, Pengaturan keseimbangan air melibatkan
interaksi antara osmotik dan volume rangsangan
Untuk peningkatan diberikan dalam osmolalitas,
peningkatan ADH plasma akan lebih besar di
hipovolemik daripada di negara-negara normovolemic
Osmoregulation of ADH release
Stimuli for ADH secretion
SELESAI