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Physiology 3 > Week 7 (kidney) physiology > Flashcards

Week 7 (kidney) physiology Flashcards

1
Q

deep anaesthesia use in rodent model studies

A

To maintain cardiovascular stability - studying kidney function
Enables:
single nephron micropuncture - test to assess how the nephron is handling fluid.

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2
Q

proximal/distal tubule and peritubular capillary

A

Tubules have anatomical proximity to capillaries.
Efficient exchange of substances between the nephron and the bloodstream

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3
Q

functional imaging of kidney (normal vs hypertension)

A

Through MRI and contrast agents injected into the blood stream.
Healthy kidneys are generally well perfused.
Kidneys suffered from hypertension will generally undergo atrophy and are not well perfused —–> non-functional

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4
Q

nocturnal dip of BP (measure)

A

Absence of nocturnal dip exists in pre-hypertension and diabetes.

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5
Q

retinal imaging and hypertension

A

Retinal capillary/arteriole changes are indicative of some diabetic and hypertensive disorders. Such as thicker arteriole walls and loss of small capillaries.

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6
Q

kidney’s perfusion

A

Kidney take 20% of the cardiac output, thus highly perfused.
But the arterial beds of the kidney are auto-regulated.

Along with brain and heart.

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7
Q

Renal autoregulation of blood flow

A

So the glomerular filtration rate is tightly regulated within physiological ranges (AUTOREGULATORY RANGE of BP (80mmHg - 180mmHg)

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8
Q

Flow can be detected using?

A

Ultrasound probes:
By measuring the frequency difference of blood flow to measure it.

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9
Q

Why is autoregulation of blood flow important?

A

So the perfusion of the organ is stable despite acute changes in blood pressure.

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10
Q

myogenic reflex of renal vasculature

A
  1. As arteriole stretches -> detected by smooth muscle cells around arteriole
  2. The stretch releases ATP (autocrine signalling)
  3. Extracellular ATP is detected by P2X1 receptor —-> increase in intracellular calcium
  4. intracellular calcium will lead to muscle cell contraction
  5. arteriole constriction
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11
Q

sensitivity of ATP of arterioles

A

Amongst:
arcuate (between medulla and cortex)
interlobular (branches from arcuate arterioles)
afferent arterioles (branches from interlobular)
Afferent arterioles are the most sensitive to extracellular ATP concentration that leads to arteriole constriction.

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12
Q

Rodent model (P2X1 KO)

A

When these receptors to ATP are knocked out, there will be no myogenic reflex.

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13
Q

oxygen gradient in the kidney

A

Highest in the cortex, lowest in the medulla (10mmHg)
This means that the cells in the medulla are very vulnerable to abnormal anaemia conditions

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14
Q

layers of glomerular filtration (from capillary blood to primary urine)

A

From capillary blood:

  1. (Capillary) Glomerular endothelial cells
  2. (Connective tissue) Glomerular basement membrane
  3. Podocytes

To Bowman’s capsule

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15
Q

Glomerular endothelial cells (permeability)

A
  1. Negatively charged
  2. HIGH permeability
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16
Q

Glomerular basement membrane (permeability)

A
  1. Has collagen and laminin, HIGHLY negatively charged
    Some proteins are negatively charged, repelled from basement membrane.
  2. HIGH permeability
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17
Q

Podocytes (which layer is it? what is it called? function?)

A
  • The last layer of the glomerular filtration
  • This is the barrier that truly controls substances that filter through.
    The cell-cell junction between foot processes of podocytes are called slit diaphragms.
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18
Q

another name for slit membrane/diaphragm

A

nephrins

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19
Q

Where are peritubular capillaries from?

A

From the efferent arteriole that continues to reabsorb substances from the renal tubules.

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20
Q

What is the molecular radius that all charges can pass through the glomerular filtration layers?

A

1.6 nm

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21
Q

How does charge affect protein filtration through the glomerulus

A

The more negatively charged, the less filterable.
The more positively charged, the more filterable.
- If the molecular radius of an anion reaches 3nm, it is not filterable at all.
For example: albumin (-ve charge and between 3-4 nm) and not filtered.

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22
Q

Reptation in glomerular filtration

A

Reptation - derived from reptile
Shape of filtered substance also matters.

23
Q

nephrin vs podocin

A

nephrins make up the slit membrane between podocytes, regulates permeability.
podocin can interact with nephrins and act as scaffolding proteins that structurally support the slit membrane.

24
Q

podocin KO consequence (mice model)

A
  • protein leakage in urine
  • decreased survival rate
25
Q

mutation in podocin and nephrin

A
  • leads to nephrotic syndrome
  • leakage of proteins to the urine.
26
Q

genetic mutations of the nephrons that lead to dehydration

A
  1. nephrogenic DI: irresponsive to ADH –> dilute urine
  2. Bartter syndrome: failure to reabsorb sodium and chloride –> excessive loss of salt and water.
27
Q

What’s another mechanism of renal autoregulation aside from myogenic reflex

A

tubuloglomerular feedback (TGF):
The tubular cells - macula densa, and the vascular cells - afferent arteriole form the juxtaglomerular apparatus.

  • Negative feedback from nephrons to afferent arteriole.
28
Q

Where is the macula densa?

A

Distal convoluted tubule

29
Q

How does the macula densa feeds back?

A

They sense the concentration of Chloride and Sodium ions, if in excess, they will feedback to the afferent arteriole.
—> paracrine signalling
—> constriction of the afferent arteriole.

30
Q

How does concentration of chloride stimulate tubuloglomerular feedback?

A

The rise in Cl- concentration is sensed by apical NKCC2 (sodium-potassium-2chloride cotransporter)
Macula densa will release ATP to constrict the afferent arteriole.

31
Q

What side is the apical membrane (tubule) facing?

A

the urine

32
Q

What side is the basolateral membrane (tubule) facing?

A

the blood

33
Q

proximal c. tubule reabsorption (iso-osmotic)

A

Reabsorbs the same amount of sodium as it does for water.
Osmolarity stays the same.

34
Q

Fanconi syndrome characteristic

A

Defect in the proximal tubule where it cannot reabsorb nutrient (glucose) or electrolytes back.

35
Q

causes of Fanconi syndrome

A

Most times drug toxicity (paracetamol, antibiotics, anti-cancer drugs)
- sometimes genetic factors.

36
Q

glomerulotubular balance (GTB) is…

A

as GFR increases, proximal tubule reabsorption increases too.
reabsorption is in proportion to GFR.

37
Q

GTB (difference from TGF)

A

glomerulotubular balance
vs
tubuloglomerular feedback
- There is limited reabsorption of the distal tubules
- distal tubules are more regulatory.
- not neuronal or hormonal, maybe through ATP.

38
Q

Principal cell (collecting tubule) channels

A

ENaC - transports Na+ from urine to epithelial cell
Na/K pump - reabsorbs Na+ from the cell to the blood in exchange with K+ using ATP hydrolysis.
ROMK - transports K+ out to the urine

39
Q

4 actions of aldosterone to ENaC

A
  1. (increase driving force) Increases turnover of Na+/K+ pump, much more efficiency, more Na+ chemical gradient —-> indirectly stimulates ENaC to reabsorb Na+ from urine.
  2. (makes more channel) via MR, stimulates transcription of 3 subunits that make up ENaC.
  3. quicker transportation of ENaC to the apical membrane (SGK1).
  4. suppresses degradation (ubiquitin ligases)

Increases K+ secretion.

40
Q

SGK1 function

A

transport ENaC to apical surface of tubule

41
Q

what kind of transporter is ENaC

A

ion channel - passive diffusion of sodium

42
Q

full name of ENaC

A

epithelial sodium channel

43
Q

Amiloride is??

A

Is an anti-hypertensive drug.
Blocks ENaC. So it increases Na+ excretion and retains K+.

44
Q

Na+ influx causes…
What can resume Na+ influx?

A
  • The influx of positive charge will reduce the electrochemical gradient for Na+ to come in.
  • Positive charge needs to go out for Na+ influx,
  • K+ goes out.
45
Q

What if the renal cell doesn’t have 11beta-HSD2?

A

Glucocorticoid, cortisol, will stimulate MR too, therefore there will be
Overactivation of ENaC from MR stimulation.
1. Hypertension.
2. Low sodium excretion
3. Much more responsive to amiloride (inhibitor of ENaC)

46
Q

function of 11beta-HSD2

A

turns cortisol to cortisone.

47
Q

Why does 11beta-HSD2 dysfunction lead to death?

A

Not from hypertension.
It’s from increased loss of potassium –> increased excitability – heart attack.

48
Q

Another mechanism that copes with high BP

A

pressure natriuresis

49
Q

health vs hypertensive people in excretion of sodium (high BP)

A

hypertensive people are less able to excrete sodium through the renal pathway to decrease BP.

50
Q

Pressure natriuresis: pathways

A

Increase in BP: aorta or renal artery pressure.
- reduction in tubular Na+ reabsorption
- an increase in urine Na excretion (natriuresis)

51
Q

How do kidneys detect high BP when it can autoregulate?

A

Cortex blood flow remains constant.
- GFR remains constant

Medullary flow increases as blood flow increases. (medulla doesn’t autoregulate)
- limited space in the renal capsule –> increased Medullary flow will lead to higher hydrostatic pressure.
- downregulates epithelial sodium transporters.

52
Q

how high BP regulates transporters

A

Increase flow or BP:
downregulate NHE (Na+/H+ exchange) and NKCC2 (Na/K/2Cl cotransporter).
- internalise NHE
- increased sodium excretion

53
Q

ATP role in pressure-natriuresis

A

stretch of afferent arteriole –> release of ATP
- ATP will downregulate NHE3 and NKCC2.
-> increased sodium excretion and relieve hypertension

54
Q

NO role in pressure-natriuresis

A
  • downregulates NKCC2 like ATP does.
  • vasodilates -> increased hydrostatic pressure to reduce Na+ reabsorption (proximal tubule) and increase natriuresis
  • Thick limb of Henle (Ca2+ influx - increase in NO): downregulate NKCC2 and Na+\K+ pump.

Physiology 3 (11 decks)

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