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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
Sensors involved in sodium reabsorption
* 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
Effector pathways in controlling sodium reabsorption
* 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
How are the renal sympathetic nerves an effector pathway for controlling Na reabsorption?
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
Intrinsic control of renin release related to juxtaglomerular feedback?
* 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
How may renin be released?
* 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
action of renin on RAAS
(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
5 effects of angiotensin II
- stimulates proximal Na+ reabsorption - stimulates ADH release - causes aldosterone secretion - causes thirst - vasoconstricts small arterioles
32
Action of angiotensin II on PCT
* 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
How does angiotensin II stimulate thirst?
• 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
Effects of aldosterone
* 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
When is aldosterone secreted?
* 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
What is released when there is a high blood volume which stretches the heart muscle?
- release of natriuretic peptides | 28 amino acids
37
Effect of NP
- increased sodium excretion in the urine | - act as natriuretics an diuretics and have hypotensive effects
38
Two types of NP
- A type secreted from atrial myocardium ANP | - B type secreted from ventricular myocardium BNP
39
Effect of NP natriuretic?
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
Diuretic effect of NP?
inhibits ADH release
41
Hypotensive effects of NP
decreases blood pressure by systemic vasodilation, increases GFR by dilating afferent arterioles
42
ANP effect
* 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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