1. Dr. Yogesh Kumar
Department Of Physiology

3.  Master coordinator of endocrine system
 Anterior ,posterior , pars intermedia
 Location
 Functions
 Development
 Hypothalamo- hypophyseal portal system

5.  Control of anterior pituitary
 Control of posterior pituitary
 Various group of nucleus
 Location
 Functions

8.  Both are synthesized in the cell bodies of
hypothalamic neurons
 ADH: supraoptic nucleus
 Oxytocin: paraventricular nucleus
 Both are synthesized as preprohormones and
processed into nonapeptides (nine amino
acids).
 They are released from the termini in response
to an action potential which travels from the
axon body in the hypothalamus

11.  In uterus during parturition
 In mammary gland during lactation

12.  suckling is major stimulus for release.
 sensory receptors in nipple connect with nerve
fibers to the spine, then impulses are relayed
through brain to PVN where cholinergic
synapses fire on oxytocin neurons and
stimulate release.

13.  Reflexes originating in the cervical, vaginal
and uterus stimulate oxytocin synthesis and
release via neural input to hypothalamus
 Increases in plasma at time of ovulation,
parturition, and coitus
 Estrogen increases synthesis and lowers
threshold for release

17.  Supraoptic nucleus
 Role in kidney
 Role in BP
 Osmoreceptors and baroreceptors

18.  It is synthesized as pre-prohormone and
processed into a nonapeptide (nine amino
acids).
 DH synthesized in the cell bodies of
hypothalamic neurons in the supraoptic nucleus
 ADH is stored in the neurohypophysis (posterior
pituitary)—forms the most readily released ADH
pool

19.  Mechanical disruption or the neurohypohyseal
tract by trauma, tumor, or surgery temporarily
causes ADH deficiency.
 ADH will be restored after regeneration of the
axons (about 2 weeks).
 But if disruption happens at a high enough
level, the cell bodies die in the hypothalamus
resulting in permanent ADH deficiency

20.  ADH is also known as arginine vasopressin
(AVP = ADH) because of its vasopressive
activity, but its major effect is on the kidney in
preventing water loss.

21.  Regulated by osmotic and volume stimuli
 Water deprivation increases osmolality of
plasma which activates hypothalmic
osmoreceptors to stimulate ADH release

23.  ADH binds to V2 receptors on the peritubular
(serosal) surface of cells of the distal
convoluted tubules and medullary collecting
ducts.
 Via adenylate cyclase/cAMP induces production
and insertion of AQUAPORIN into the luminal
membrane and enhances permeability of cell to
water.
 Increased membrane permeability to water
permits back diffusion of solute-free water,
resulting in increased urine osmolality
(concentrates urine).

24.  Regulated by osmotic and volume stimuli
 Water deprivation increases osmolality of plasma
which activates hypothalmic osmoreceptors to
stimulate ADH release

28.  The two major stimuli of ADH secretion
interact.
 Changes in volume reinforce osmolar
changes.
 Hypovolemia sensitizes the ADH response
to hyperosmolarity.

29.  ADH action in the kidney is mediated by its
binding to V2 receptors, coupled to adenylate
cyclase and cAMP production.
 cAMP activates protein kinase A which prompts
the insertion of water channels into the apical
membrane of the cell.
 When ADH is removed, the water channels
withdraw from the membrane and the apical
surface of the cell becomes impermeable to
water once again. .

30.  This mechanism of shuttling water channels into
and out of the apical membrane provides a very
rapid means to control water permeability
 The basolateral membrane of the ductal cells
are freely permeable to water, so any water that
enters via the apical membrane exits the cell
across the basolateral membrane, resulting in
the net absorption of water from the tubule
lumen into the peritubular blood.

31.  Water deprivation stimulates ADH secretion,
decreases free-water clearance, and
enhances water conservation.
 ADH and water form a negative feedback
loop.

32.  ADH deficiency is caused by destruction or
dysfunction of the supraoptic and
parventricular nuclei of the hypothalamus.
Inability to produce concentrated urine is a
hallmark of ADH deficiency and is referred to
as diabetes insipidus.
 ADH also acts on the anterior pituitary to
stimulate the secretion of ACTH.