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Endocrinology > Hypothalamo-neurohypophysial system > Flashcards

Hypothalamo-neurohypophysial system Flashcards

1
Q

What is the neurohypophysis made of?

A

nerve axons that pass down from the pituitary stalk

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2
Q

What is the suprachiasmatic nucleus?

A

vasopressinergic neurones originate here

location of biological clock

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3
Q

What are magnocellular neurones?

A 
cell bodies in paraventricular/supra optic nucleus
terminate in neurohypophysis
large long axons 
to posterior pituitary 
vaso/oxytocinergic
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4
Q

What are parvocellular neurones?

A 
cell bodies in PV nuclei
terminate in median eminence and other parts of brain
average, short axons 
to anterior pituitary
vaso/oxytocinergic
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5
Q

What neurones are found in the paraventricular nuclei?

A

parvocellular and magnocellular neurones
parvocellular produce CRH and vasopressin
most magnocellular and terminate in NH
some are parvocellular and terminate in ME

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6
Q

What neurones are found in the supraoptic nuclei?

A

all magnocellular neurones

pass through ME and terminate in NH

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7
Q

What are Herring bodies?

A

areas where neurosecretions are stored on way down to neurohypophysis
specific to magnocellular neurones of PV and SO nuclei

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8
Q

Why are neurosecretions hormones?

A

they are released into the general circulation

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9
Q

What 2 hormones are both released from paraventricular neurones?

A

CRH and vasopressin from parvocellular neurones terminating in ME and travel down pituitary portal system into pituitary corticotrophs
both secreted at same anatomical location

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10
Q

What does CRH need to effectively stimulate ACTH release?

A

vasopressin

vasopressin is not an ACTH secretogogue on its own

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11
Q

What is a secretogogue?

A

a substance that promotes secretion

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12
Q

What generates pre-provasopressin?

A

nucleus

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13
Q

What does signal do to pre-provasopressin?

A

directs it to the axons where it forms a pro-hormone

pre-provasopressin splits in 2

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14
Q

What happens to pre-provasopressin?

A

converted to pro-hormone –> vasopressin + neurophysin + glycopeptide

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15
Q

What is AVP?

A

arginine vasopressin

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16
Q

What is neurophysin?

A

large molecule (protein) specific to provasopressin

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17
Q

What is GP ?

A

glycopeptide

= a prolactin releasing factor

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18
Q

What is the difference with oxytocin compared to vasopressin production?

A

different neurophysin produced and no glycopeptide

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19
Q

What happens to vasopressin pro-hormone?

A

passes along neurone in Herring bodies
neurophysin bound gives stability and prevents hormone diffusing out of Herring body and being degraded by enzymes
at end of neurone the pro hormone is cleaved

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20
Q

What are the differences in structure of vasopressin and oxytocin?

A

AVP has Phenylalanine not isoleucine
AVP has arginine instead of leucine
DIFFER BY TWO AMINO ACIDS

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21
Q

What vasopressin do some animals have?

A

lysine instead of arginine

22
Q

What are the similarities between vasopressin and oxytocin?

A

nonapeptides

both synthesised as pro hormones which as cleaved to form hormone and neurophysin protein

23
Q

What is the effect of vasopressin on renal collecting ducts?

A

stimulate water reabsorption

anti diuretic effect

24
Q

What is effect of vasopressin on blood vessels?

A

vasoconstriction

VP released by parvocellular neurones in ME and acts with CRH to control corticotrophin release

25
Q

What is the effect of VP on CNS?

A

acts as hormone/NT affecting behaviour

26
Q

What is the effect of VP on synthesis of blood clotting factors?

A

involved in clotting factors VIII and VWF

analogues of VP and VP used to treat blood clotting disorders

27
Q

What is the effect of VP on hepatic glycogenolysis?

A

VP released by stressors (dehydration)

increases blood glucose

28
Q

Where are V1a VP receptors?

A

most important in vasculature, brain mainly
arterial/olar smooth muscle - vasoconstrict
hepatocytes - glycogenolysis
CNS neurones - behavioural and other effects

29
Q

Where are V1b VP receptors? (V3)

A

adenohypophysial corticotrophs (ACTH production)

30
Q

Where are V2 VP receptors?

A

collecting duct cells - water reabsorb
endothelial cells - vasodilation
factor VIII and VWF

31
Q

How does a V1 receptor work?

A 
Gq protein linked receptor
protein is linked to phospholipase C
PLC activated
convert PIP3 to IP3 and DAG
these both increase [Ca] cytoplasm 
activate protein kinase C
32
Q

How does a V2 receptor work?

A 
Gs protein linked receptor
linked to adenylate cyclase
AC activated 
convert ATP to cAMP
activated PKA
this activates other intracellular mediators that produce cellular responses - recruit aquaporins to cause ADH effect
33
Q

How to hormones affect the brain?

A

if enter CSF

34
Q

How does vasopressin work in the principal cells?

A
  1. V2 receptors on basolateral membrane bind to VP and activate AC
  2. AC converts ATP –> cAMP
  3. cAMP activated PKA
  4. stimulates AQP2 synthesis
  5. AQP2 needed to move water across cell membrane
  6. AQPs assemble into accumulations called aggraphores
  7. VP causes these to migrate to apical membrane (face inside of collecting duct)
  8. Water moves into cells via AQP2
  9. Water moves out of cells by AQP3 and 4
35
Q

What are the principal cells?

A

collecting duct cells

36
Q

How many different AQPs are there?

A

9

AQP2 is VP dependent

37
Q

What is needed to move water from collecting duct –> principal cells –> blood?

A

osmotic gradient

38
Q

How is VP controlled?

1. stimulus = dehydration

A
  1. increase in plasma osmolarity detected by osmoreceptors
  2. stimulate vasopressinergic neurones to release VP
  3. more water reabsorbed and osmolarity returns to normal
  4. stimulus removed
  5. VP switched off
39
Q

What must osmoreceptors be in contact with?

A

vasopressinergic neurones in order to stimulate them

osmoreceptors are also in the blood and so lie outside the blood brain barrier (circumventricular organs)

40
Q

How is VP controlled?

2. ?

A

Influence from higher centres

  • stress
  • surgery
  • anaesthesia
41
Q

How is VP controlled?

3.?

A
  1. fall in arterial BP detected by baroreceptors
  2. activity of baroreceptors is reduced - removal of tonic inhibition of VP release
  3. baroreceptors decrease activity
  4. decreased inhibition
  5. increase VP release
  6. increase sympathetic activity (baroreceptors linked to SNS to control vasoconstriction)
  7. increase vasoconstriction –> increase BP
42
Q

What are baroreceptors?

A

stretch receptors that detect increase pressure

43
Q

What happens normally to VP?

A

tonic inhibition of VP release

44
Q

What is oxytocin?

A

a contractor hormone -cause constriction

45
Q

What is the central effect of oxytocin?

A

behavioural

46
Q

What is the effect of oxytocin on the uterus at parturition?

A 
increased stress on uterine wall 
causes release of oxytocin
acts on smooth muscle receptors on myometrial cells
contraction
facilitates delivery
47
Q

What is the effect of oxytocin on the breast during lactation?

A

prolactin stimulates milk production NOT EJECTION
ducts/alveoli that produce milk surrounded by contractile myoepithelial cells that have myoepithelial receptors

suckling –> stimulate oxytocin release –> myoepithelial cells contract –> milk ejection

48
Q

What is the difference between prolactin and oxytocin?

A

act via same afferent pathway (detection of suckling)
one arc goes to adenohypophysis to stimulate prolactin production whilst the other goes to neurohypophysis to stimulate production of oxytocin

49
Q

What is diabetes insipidus?

A

central diabetes insipidus - no VP produced
nephrogenic DI - tissue insensitivity

present with polydipsia, polyuria

50
Q

What is SIADH?

A

too much ADH produced
decrease plasma osmolarity
urine is very concentrated

Endocrinology (13 decks)

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