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Physiology and Pharmacology > Body Fluids (vasopressin) > Flashcards

Body Fluids (vasopressin) Flashcards

1
Q

what is vasopressin?

A
  • antidiuretic hormone which regulates body fluid osmolality and conserves H2O
  • it is released when the body wants to save water, so less water is lost in urine
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2
Q

how is vasopressin released?

A
  • released from posterior pituitary and secretory neurons in the hypothalamus from cell bodies
  • when there is an AP, this causes fusion of vesicles containing vasopressin with the membrane
  • vasopressin is then released into the capillaries
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3
Q

what is osmolality?

A

the concentration of body fluids

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4
Q

how does vasopressin levels affect osmolality?

A

increase in vasopressin = increase in osmolality
- more water is conserved so there is less water excreted in urine

decrease in vasopressin = decrease in osmolality
- less water is conserved so there is more water excreted in urine

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5
Q

what are hypothalamic osmoreceptors?

A
  • receptive to changes in osmolality
  • detect a change of ± 3 mosmol/kg H2O (very sensitive)
  • 1% change in osmolality leads to activation of osmoreceptors
  • located in the supra-optic and paraventricular nuclei in hypothalamus
  • when osmoreceptors are activated, there is an increase in osmolality
  • they make you feel thirsty
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6
Q

how is an increased release of vasopressin caused?

A
  • solute ingestion or H2O deficiency leads to release of vasopressin
  • stress and drugs: nicotine, ecstasy etc stimulate vasopressin release so more water retention
  • leads to a rise in osmolality
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7
Q

how is a decreased release of vasopressin caused?

A
  • excessive fluid ingestion so less vasopressin is released
  • drugs: alcohol inhibits release of vasopressin, so body excretes water when it shouldn’t be excreting water - leads to headache and dry mouth
  • more water is lost in urine due to excess water diluting the plasma
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8
Q

what is the relationship between plasma osmolality and vasopressin?

A
  • as plasma osmolality rises, there is more vasopressin released to conserve more water
  • as plasma osmolality decreases, less vasopressin is released as the body must excrete the excess water in the plasma
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9
Q

what is the relationship between urine osmolality and vasopressin?

A
  • the higher the urine osmolality, the lower the volume of water excreted in the urine
  • vasopressin release is inhibited so urine osmolality can fall and more water is excreted
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10
Q

what occurs in the principal cell of the collecting duct under the influence of vasopressin?

A 
Apical membrane = AQP2
Basolateral membrane = AQP3 and AQP4
Vasopressin 2 (V2) receptor on basolateral membrane
  1. Vasopressin activates V2 and stimulates PKA
  2. PKA phosphorylates and causes insertion of vesicles carrying AQP2 to apical membrane
  3. causes increase in AQP2s on apical membrane so there is more water reabsorption
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11
Q

how does an increase in vasopressin affect AQP2 and water conservation?

A
  • when vasopressin levels are high, there are lots of AQP2s
  • this causes more reabsorption of water and so an increased conservation of water
  • less water is lost in the urine

Net effect of increased vasopressin:

  • increased reabsorption of water
  • fall in body fluid osmolality
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12
Q

how does an decrease in vasopressin affect AQP2 and water conservation?

A
  • when vasopressin levels decrease, there are less AQP2 channels transported to the apical membrane as the vesicles take them away
  • less water reabsorption

net effect of decreased vasopressin:

  • decreased reabsorption of water
  • rise in body fluid osmolality
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13
Q

what is diabetes insipidus?

A

copious quantities of diluted urine is excreted (23L/day) - too much water excreted in urine

2 types:

  • central DI
  • nephrogenic DI
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14
Q

what is central diabetes insipidus?

A
  • no release of vasopressin
  • kidneys can respond to vasopressin, but body cannot produce it
  • less water conservation so more water lost in urine

treatment: nasal spray DDAVP (synthetic vasopressin)

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15
Q

what is nephrogenic diabetes insipidus?

A
  • lack of kidney response to vasopressin
  • due to a mutation in the V2 gene coding for the V2 receptor, or a mutation in AQP2

range of treatments

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16
Q

what is aldosterone?

A
  • released from zona glomerulosa layer of the adrenal cortex

- mineralocorticoid hormone which regulates plasma Na+, K+ and body fluid volume

17
Q

when is aldosterone released?

A

in response to:
1. Increase in plasma K+ by 0.1mM

  1. Decrease in plasma Na+
    - minor concentration maintained by osmoregulation
    - Na+ is a key component in determining osmolality and vasopressin release
  2. decrease in ECF volume
    - via renin-angiotensin system
18
Q

what does aldosterone act on?

A
  • late distal tubule
  • collecting duct
  • acts on principal cells and intercalated cells
19
Q

what does aldosterone promote?

A
  1. increased absorption of Na+
  2. increased absorption of H2O
  3. increased secretion of K+ and H+
20
Q

what is the effect of aldosterone on the principal cell?

A

called genomic action:

  • aldosterone is a steroid hormone, so is lipid soluble and can diffuse into the cell
  • cytosolic mineralocorticoid receptors in cell bind to aldosterone
  • aldosterone moves to nucleus of cell and stimulates RNA transcription and protein synthesis
  1. produces ENaC for sodium reabsorption
  2. produces ROMK for potassium secretion
  3. produces sodium-hydrogen exchanger to absorb sodium and secrete hydrogen
21
Q

what effect does aldosterone have on ENaC proteins?

A
  • non-genomic action of keeping ENaC proteins open and increase their activity for around 30 mins
  • enables more reabsorption of Na+, and therefore absorption of water too

open probability = how often Na+ channel is open

the more aldosterone, the more open ENaC on apical membrane for more Na+ absorption

22
Q

what is the effect of aldosterone on alpha-intercalated cells?

A
  • increase in protein synthesis

- formation of hydrogen-ATP channel on apical membrane so hydrogen is secreted into tubular fluid and excreted in urine

23
Q

what is the net effect of aldosterone on principal and intercalated cells?

A
  1. Increase in plasma Na+
  2. decrease in plasma K+
  3. decrease in plasma H+
  4. increase in ECF volume
24
Q

what are the problems in Liddle’s syndrome?

A
  1. Hypertension
    - high Na+ reabsorption at collecting duct, even though aldosterone levels are low
    - low aldosterone breaks its link with ENaC
    - too many open ENaC channels on apical membrane due to slowing down of endocytosis of the channels
  2. Pseudohypoaldosteronism
    - salt loss but high aldosterone
    - mutation in mineralocorticoid receptor which can no longer respond to high aldosterone
    - loss in response to aldosterone
25
Q

what does the renin-angiotensin system regulate?

A
  1. body fluid volume
  2. plasma Na+
  3. plasma K+
26
Q

where is renin released from?

A

the juxtaglomerular apparatus (JGA)

27
Q

what is the juxtaglomerular apparatus?

A
  • filtrate moves from afferent arteriole, into BC, to glomerulus then though efferent arteriole
  • proximal to loop of henle
  • macula densa releases chemicals that controls delivery of plasma to glomerular capillary bed
  • controls renin release
  • stretch receptors in afferent arterioles
  • granular cells in afferent contains packets of renin which are released into plasma, leading to cascade
28
Q

what happens during the renin-angiotensin cascade?

A
  1. decrease in ECF volume causes JGA to release renin
  2. renin activates angiotensinogen to angiotensin I
  3. angiotensin I is converted to angiotensin II by ACE
    - angiotensin II is the active component of the cascade
29
Q

what are the actions of angiotensin II?

A
  1. causes zona glomerulosa to release aldosterone when blood volume drops
  2. causes arterioles to vasoconstrict to increase blood pressure

too much angiotensin II causes increased BP and accumulation of aldosterone, so ACE inhibitors are used to prevent thus

30
Q

what is the net effect of angiotensin II?

A
  1. increase plasma Na+
  2. secretion of K+ and H+
  3. increase in ECF volume
  4. increase in blood pressure
31
Q

how can vasopressin system be reset depending on the needs of the body?

A
  • ingestion of salt leads to increase in plasma Na+, so water is absorbed into plasma and increases ECF volume
  • this inhibits release of aldosterone, so there is a loss of Na+ and water reabsorption, which lowers ECF volume
  • loss of ECF volume causes trafficking of AQP2 to apical membrane to increase water reabsorption and decrease plasma osmolality
  • this leads to release of aldosterone and resetting of vasopressin
32
Q

what is key in determining osmolality?

A

volume:

  • body resets vasopressin and controls osmolality, leading to control of volume and blood pressure
  • volume depletion stimulates release of aldoesterone and then vasopressin to raise ECF volume via reabsorption of water

Physiology and Pharmacology (13 decks)

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