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Urinary System > Regulation of Osmolarity > Flashcards

Regulation of Osmolarity Flashcards

1
Q

What is water regulation controlled by?

A

ADH (vasopressin) = arginine vasopressin (AVP)

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2
Q

Describe ADH

A

Polypeptide synthesised in the supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus in the brain
Posterior pituitary hormone
Half life around 10 mins

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3
Q

What is the primary control of ADH secretion?

A

Plasma osmolarity

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4
Q

What happens when OP of plasma increases?

A

The rate of discharge of ADH secretin neurons in SO and PVN is increased
So increased release of ADH from posterior pituitary

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5
Q

What are changes in neuronal discharge mediated by?

A

Osmoreceptors in anterior hypothalamus close to SO and PVN
Other receptors in lateral hypothalamus mediate thirst

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6
Q

What happens if there is an increase in osmolarity?

A

Increased H2O out of cell
Cell shrinks so stretch sensitive ion channel activated
Increased neural discharge

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7
Q

What happens if there is a decrease in osmolarity?

A

H2O enters cells
Cells swell
Decreased neuronal discharge
Decreased ADH secretion

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8
Q

What does change in volume of osmoreceptors do?

A

Changes in osmoreceptor discharge - stretch sensitive ion channels

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9
Q

What is normal plasma osmolarity?

A

280-290mOsm/kg H2O
Regulated very precisely

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10
Q

What is the plasma osmolarity control of ADH described as?

A

High gain - 2.5% increase in osmolarity can produce 10x increase in ADH
Very sensitive

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11
Q

Why does an increase in osmolarity that does not cause increase in tonicity is ineffective?

A

Solutes that can penetrate membranes move together with water and don’t produce osmotic drag or tonicity

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12
Q

Describe what an increase in urea causes to volume and ADH release

A

No change in volume, discharge or ADH release as urea is an ineffective osmole as no tonicity

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13
Q

What happens if increased osmolarity and NaCl?

A

Decreased volume
Increased discharge and ADH release
So water moves out

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14
Q

What does the amount of urine produced depend on?

A

Conc. of ADH
Amount of solute excreted

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15
Q

What does the ingestion of hypertonic solutions like seawater do?

A

Increase the solute load to be excreted which increases urine flow leading to dehydration as more H2O s required to excrete the solute load

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16
Q

What does urine osmolarity depend on?

A

Reabsorption in the collecting duct

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17
Q

What happens after vasopressin binds to the membrane receptor?

A

Receptor activates cAMP second messenger system
Cell inserts AQP2 water pores into apical membrane
Water is absorbed by osmosis into blood

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18
Q

How is there increased permeability of collecting ducts to H2O?

A

By incorporating H2O channels into luminal membrane - aquaporins

19
Q

What happens to cortical CD if ADH is present?

A

H2O able to leave CD so cortical CD becomes equilibrated with cortical interstitium - 300mOsm/l
CD passes through hypertonic medullary interstitial gradient created at loop of Henle

20
Q

What happens if there is maximum conc. of ADH?

A

Produces small volume of highly concentrated urine which contains less H2O than solute which compensates for water deficit
Adds pure H2O to ECF as reabsorbed by high oncotic pressure in vasa recta

21
Q

What happens in the absence of ADH?

A

CD are impermeable to H2O so medullary interstitial gradient is ineffective in movement of H2O - large volume dilute urine is excreted
mOsm/l can fall to 30-50

22
Q

What is the role of urea?

A

Plays role in production of concentrated urine
In presence of ADH, movement of H2O out of CD concentrates the urea in ducts

23
Q

Is urea permeable in CD?

A

Relatively permeable - particularly towards medullary tips
As approached medullary tips - increasing tendency to move out down conc. gradient

24
Q

What is permeability of late medullary CD enhanced by?

A

ADH

25
Q

Describe urea during anti-diuresis

A

High levels of ADH - urea reabsorbed from CD into interstitium where acts to reinforce interstitial gradient in ascending loop of Henle

26
Q

Why is urea retained in anti-diuresis?

A

Order to save water and reinforce medullary gradient in region of thin ascending limb of Loop of Henle
Uraemia occurs

27
Q

What would happen if urea is not reabsorbed in the tubule?

A

It would exert osmotic effect to hold H2O in tubule and therefore reduce potential for rehydration

28
Q

Why is reabsorption of urea possible at any level of ADH?

A

So that CD permeability of CD can be precisely graded to meet demands of body for H2O regulation

29
Q

What is the ECF volume effect on ADH secretion?

A

Increase ECF volume - decrease ADH secretion
Decrease ECF volume - increase ADH secretion

30
Q

What is the relationship between ECF volume and ADH secretion?

A

Inverse relationship between rate of ADH secretion and rate of discharge of stretch receptor afferents in low and high pressure areas of circulation

31
Q

Where are low pressure receptors located?

A

L and R atria and great veins

32
Q

Where are high pressure receptors located?

A

Carotid and aortic arch baroreceptors

33
Q

What do moderate decreases in ECF volume primarily effect?

A

Atrial receptors
Decrease atrial receptor discharge so increase ADH release
Normally exert tonic inhibitory discharge of ADH secretion via vagus nerve

34
Q

What receptors are involved if volume changes enough to affect MBP?

A

Carotid receptors which also contribute to ADH secretion

35
Q

What happens to ADH release when going from lying down to standing up?

A

Increase ADH release

36
Q

What are ADH secreting cells?

A

Neurons
They receive multiple inputs which they integrate to determine ADH conc.

37
Q

What stimuli increase ADH?

A

Pain, emotion, stress, exercise, nicotine, and morphine
Also following traumatic surgery

38
Q

What stimuli supresses ADH release?

A

Alcohol

39
Q

What is central diabetes insipidus?

A

Hypothalamic areas synthesizing ADH become diseased due to tumours, meningitis or damaged in surgery

40
Q

What is peripheral diabetes insipidus?

A

CD is insensitive to ADH

41
Q

What are patient with DI characterised by?

A

Passage of large volumes of very dilute urine
>10l/day and they drink large volumes of water

42
Q

What is the treatment for DI?

A

Central - ADH
Peripheral - Fix ion disorders (hypercalcaemia and hypokalaemia) as cant give ADH

43
Q

What are the changes in volume of fluid along the nephron?

A

Bowman’s - 180l/day
End of proximal tubule - 54l/day
End of loop of Henle - 18l/day
End of CD - 1.5l/day

44
Q

What are the changes in osmolarity along the nephron?

A

Bowman’s - 300mOsm
End of proximal tubule - 300
End of loop of Henle - 100
End of CD - 50-1200

Urinary System (26 decks)

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