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CVR > Kidney function IV > Flashcards

Kidney function IV Flashcards

1
Q

What is the normal range for plasma osmolality?

A

285-295 mosmol/kg

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2
Q

At what levels does hyperkalaemia occur?

A

Plasma [K+] concentration > 5.5mM

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3
Q

Where are ROMK channels expressed?

A

In the principal cells of the collecting duct

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4
Q

What does ECF refer to?

A

Plasma in vascular system and interstitial fluid that surrounds the cells

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5
Q

What can increase the ECF osmolarity?

A
  • water deprivation
  • solute ingestion
  • diarrhoea
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6
Q

What receptors detect an increase in osmolarity?

A

osmoreceptors located close to the supraoptic and paraventricular nuclei in the hypothalamus of the brain

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7
Q

Effect of stimulating osmoreceptors

A
  • send signals to posterior pituitary gland to release ADH into the blood
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8
Q

What does ADH do?

A

Makes the cells of the collecting duct more permeable to water causes water retention by the kidneys

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9
Q

What level of osmolarity do the lateral preoptic receptors detect?

A

changes in osmolarity > 295 mosm/l

Cause a thirst

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10
Q

What decreases ECF osmolarity

A

excessive fluid ingestion

  • detected by the osmoreceptors in the supraoptic and paraventricular nucleus of the hypothalamus to suppress ADH release from posterior pituitary
  • to make cells of the CD impermeable to water
  • more water excretion via the kidneys–> diuresis

Osmoreceptors in the lateral pre-optic area suppress thirst

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11
Q

How is the volume of ECF regulated?

A
  • osmolarity of ECF is tightly controlled
  • volume of ECF is determined by the volume of solute (mainly NaCl)
  • regulation of volume is all about sodium balance
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12
Q

Quantity of dietary salt intake?

A

Intake varies from 0.05-25g/day

Average salt intake is 2.3g/day

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13
Q

What is an important determinant of blood pressure in the veins, cardiac chambers and arteries?

A

plasma volume!!

low total body sodium –> low plasma volume –> low cardiovascular pressures

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14
Q

Size of intracellular fluid compartment?

A

twice the size of ECF

10L of interstitial fluid + 4L of plasma

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15
Q

Main solute in ECF and ICF

A

sodium in ECF

potassium in ICF

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16
Q

Through what organ does the body directly control osmolarity and volume of ECF in vascular system?

A

kidneys

affects the osmolarity and volume of other compartments

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17
Q

What do osmoreceptors control?

A
  • water renal excretion by altering ADH release

- water intake by altering thirst

18
Q

Equation for amount of sodium excreted?

A

sodium excreted= sodium filtered- sodium reabsorbed

19
Q

How does the kidney control Na+ content?

A

By controlling GFR and sodium reabsorption

regulate them separately

20
Q

What process is frequently ignored?

A
  • small passive secretion process of Na in the descending limb of the loop of Henle
21
Q

What does the GFR depend on?

A
  • combination of opposing starling forces (hydrostatic and colloid osmotic)
  • hydraulic permeability
  • characteristics of capillaries
  • surface area

regulated by both neural and hormonal input

can be controlled extrinsically and intrinsically

22
Q

What reduces the GFR

A
  • constricting afferent arteriole
  • decreases blood flow
  • decreases hydrostatic pressure gradient
  • reduces GFR
23
Q

Describe the extrinsic control of GFR to maintain systemic blood pressure.

A
  • Activation of sympathetic nervous system (baroreceptor response- stretch receptors in carotid and aortic sinus)
  • If there is a decrease in stretch, they will send signals to the cardiovascular centre in the brain which activates the sympathetic nervous system
  • SN vasoconstricts afferent arteriole which reduces GFR
  • Reduces surface area of filtration barrier via mesangial cells which reduces GFR
  • ^ activates the mesangial cells that lie over the glomerular capillaries- when activated the actin contract reducing the SA of filtration barrier
  • Also increases renin release
  • Reduction in GFR will conserve sodium and water and increase blood volume/ pressure!!
  • As tubular flow has decreased, it allows time for Na and water reabsorption processes to occur
24
Q

Describe the intrinsic control of GFR to protect capillaries from hypertensive damage and increase blood volume/ pressure

A

Autoregulation’ within the kidney can control afferent arteriole constriction
• Mechanisms include
o Myogenic response by the renal smooth muscle cells that surround arterioles (vasoconstriction in response to stretch)
o Tubuloglomerular feedback by the juxtaglomerular apparatus (controls vasoconstriction of AA and renin release)

  • Renal blood flow (RBF) and GFR remain constant for arterial pressures between 90- 200 mmHg
  • Afferent arterioles constrict when BP is raised and dilate when BP is lowered, thus maintaining constant capillary pressure and glomerular blood flow.
  • Purpose: to protect glomerular capillaries from hypertensive damage and maintain a healthy GFR.
25
Q

Sensors involved in sodium reabsorption

A
  • Tubular fluid NaCl concentration receptors within macula densa.
  • Pressure receptors (baroreceptors) in central arterial tree.
  • Pressure receptors in renal afferent arterioles (intrarenal baroreceptors).
  • Volume receptors in cardiac atria and intrathoracic veins.
26
Q

Effector pathways in controlling sodium reabsorption

A
  • Renal sympathetic nerves (stimulate renin release)
  • Direct pressure effect on kidney
  • Renin/angiotensin II/aldosterone (stimulate Na+ reabsorption)
  • Atrial Natriuretic Peptide (causes natriuresis (increased Na+ excretion in urine), inhibits Na+ reabsorption)
  • Dopamine (causes natriuresis, inhibits Na + reabsorption)
27
Q

How are the renal sympathetic nerves an effector pathway for controlling Na reabsorption?

A

Activation of sympathetic nervous system
• Vasoconstricts afferent arteriole so reducing GFR
• Reduces surface area of filtration barrier via mesangial cells reducing GFR
• Stimulates renin release

Sympathetic nerves of granular cells receive signals from baroreceptors in central arterial tree via cardiovascular centre.
• Sympathetic nerve fibres innervates the granular cells of the juxtaglomerular cells
• Juxtaglomerular cells found in the walls of the afferent arteriole
• Inc in activity causes the release of renin into blood of AA
• Is an extrinsic control of renin release

28
Q

Intrinsic control of renin release related to juxtaglomerular feedback?

A
  • Macula densa cells in walls of tubules
  • Opposing these are the juxtaglomerular cells in the juxtaglomerular apparatus
  • Increased sodium delivery to macula densa cells, will cause soidum reabsorption to occur
  • Activity of NaKATPase pump on basolateral membrane will be increased
  • As a result of ATP hydrolysis to ADP, will generate adenosine
  • Adenosine will work through A1 receptors which are found on the granular and vascular smooth muscles in walls of AA to cause an increase in calcium concentration
  • Increase in calcium concentration causes vasoconstriction and a decrease in renin release
29
Q

How may renin be released?

A
  • Decrease in sodium delivery ( is a combination of concentration and tubular flow rate) to macula densa cells
  • Decrease in wall tension in the afferent arteriole (intrarenal baroreceptor) e.g. drop in mean or pulse pressure
  • Increase in sympathetic activity (baroreceptor response to low BP)
30
Q

action of renin on RAAS

A

(57 kilodalton peptide called angiotensinogen present in the plasma in excess, synthesised by the liver)

  • renin causes the breakdwon of angiotensinogen to angiotensin I
  • when angiotensin I circulates the blood, will be exposed to the luminal wall of capillaries
  • so ACE breaks it down to angiotensinogen Ii
31
Q

5 effects of angiotensin II

A
  • stimulates proximal Na+ reabsorption
  • stimulates ADH release
  • causes aldosterone secretion
  • causes thirst
  • vasoconstricts small arterioles
32
Q

Action of angiotensin II on PCT

A
  • There are angiotensin II type 1 receptors expressed on luminal membrane and basolateral membrane of tubular epithelium
  • Angiotensin II stimulates PCT Na+ reabsorption by binding to these receptors and stimulating the activity of the Na:H exchanger and Na:K:ATPase pump
33
Q

How does angiotensin II stimulate thirst?

A

• Angiotensin II binds to angiotensin II receptors on the organum vasculosum lamina terminalis, median preoptic nucleus and the subfornical organ which doing so stimulates ADH release and in a separate reaction causes thirst

34
Q

Effects of aldosterone

A
  • Aldosterone is released form the outer tissue region of the adrenal gland/ secreted by the zona glomerulosa in adrenal cortex
  • Causing an increase in sodium reabsorption in DCT and CD
  • Increasing Na reabsorption increases water reabsorption by osmoregulation
  • Resulting in an expansion of ECF and a restoration of ECF volume
  • Aldosterone also increases Na+ reabsorption from sweat glands and salivary glands and increases Na+ ABSORPTION from the gut
35
Q

When is aldosterone secreted?

A
  • Is secreted due to the presence of angiotensin II and due to increased plasma K+ concentration
  • Is a steroid hormone and will bind to nuclear receptors and stimulate protein synthesis
  • Its actions are much slower compared with ADH
  • Main action is on the principal cells of the collecting duct where it stimulates Na+ reabsorption by stimulating production of NaK pumps and epithelial Na+ channels (ENaC)
  • Water follows Na
36
Q

What is released when there is a high blood volume which stretches the heart muscle?

A
  • release of natriuretic peptides

28 amino acids

37
Q

Effect of NP

A
  • increased sodium excretion in the urine

- act as natriuretics an diuretics and have hypotensive effects

38
Q

Two types of NP

A
  • A type secreted from atrial myocardium ANP

- B type secreted from ventricular myocardium BNP

39
Q

Effect of NP natriuretic?

A

act on CD cells to inhibit Na+ entry through ENaC, inhibits renin release and aldosterone production. Synergism with dopamine to inhibit Na+K+ ATPase activity in PCT

40
Q

Diuretic effect of NP?

A

inhibits ADH release

41
Q

Hypotensive effects of NP

A

decreases blood pressure by systemic vasodilation, increases GFR by dilating afferent arterioles

42
Q

ANP effect

A
  • ANP inhibits Na+-K+ ATPase pump activity and promotes dopamine entry into the proximal tubule epithelium via OCT (organic cation transporter).
  • Dopamine then enters the tubule lumen via OCTN (L- carnithine/organic cation transporter) and then contributes to inhibiting Na+-K+ ATPase pump activity.
  • Synergy- purpose is to inhibit Na+ (and water) reabsorption.
  • End result: Natriuresis

CVR (12 decks)

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