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Kidney physiology > Regulation of salt and water balance > Flashcards

Regulation of salt and water balance Flashcards

1
Q

What two interlinked changes affect the osmolarity and volume of plasma?

A

Na+ excretion

H2O excretion

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2
Q

How are changes in blood volume detected (5)?

A

Altered sympathetic discharge

Baroreceptors detect changes in circulating blood volume.

Cardiac filling

Renal afferent arterioles (stretch receptors)

Renal blood flow causes changes in NaCl delivery to macula densa

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3
Q

How are changes in blood osmotic potential detected?

A

Osmoreceptors in the hypothalamus

Alterations in NaCl delivery to macula densa cells

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4
Q

How do baroreceptors detect changes in blood volume?

A

The baroreceptors are stretch-sensitive mechanoreceptors.

At low pressures, baroreceptors become inactive and firing frequency stops.

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5
Q

What is the effect of decreased baroreceptor firing frequency?

A

Sympathetic system becomes active, which stimulates renin production at the JGA (RAAS).

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6
Q

How do cardiac stretch receptors detect changes in blood volume?

A

Low pressure baroreceptors (stretch receptors) in the wall of the atria.

When blood volume is low, there is less stimulation of these receptors

When blood volume is high there is more stimulation of receptors

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7
Q

Which baroreceptors are the most sensitive?

A

Low pressure baroreceptors (stretch receptors) in the wall of the atria.

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8
Q

What is the effect of decreased firing frequency from cardiac stretch receptors?

A

Increases sympathetic drive to the JGA of the kidney - stimulate renin production

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9
Q

What is the effect of increased firing frequency from cardiac stretch receptors?

A

The receptors signal for the release of ANP, which acts to antagonise RAAS.

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10
Q

What is the effect of decrease in arterial pressure at the level of the afferent arteriole?

A

Renal stretch receptors trigger renin secretion

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11
Q

What is the % contribution of osmoreceptors to ADH release?

A

2%

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12
Q

How does low blood volume affect the bodies sensitivity to osmotic changes?

A

Increases it

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13
Q

Where are osmoreceptors?

A

Hypothalamus (paraventricular nucleus and supraoptic nucleus)

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14
Q

Are osmoreceptor cells permeable to water? How?

A

Yes, AQP4

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15
Q

How does increase in plasma osmolarity cause vesicular release of ADH (osmoreceptors)?

A

Plasma osmolarity rises

Water moves out of the cell due to osmosis

Stretch inactivated cation channels (SICs), open when cell shrinks

Allow Na+ / K+ ions to enter the cell.

Depolarisation activates voltage-gated sodium channel - further depolarisation and action potential

Action potential causes the opening of VGCC - Ca2+ influx.

Causes the vesicular release of ADH from the posterior pituitary gland.

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16
Q

How does an increase in circulating volume affect rate of sodium delivery to macula densa cells?

A

Increased GFR means that there is an increased rate of Na+ delivery to MD

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17
Q

How does a decrease in circulating volume affect rate of sodium delivery to macula densa cells?

A

Decreased GFR means that there is an decreased rate of Na+ delivery to MD

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18
Q

How can a low GFR fed-back and be regulated?

A

Low GFR decreases Na+ delivery to MD, feedback therefore leads to renin release.

RAAS - efferent arteriole vasoconstriction to increase GFR

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19
Q

Why are starling forces very important in sodium reabsorption?

A

Changes to the starling forces in the PCT ensure that, even if GFR changes, reabsorption at the PCT will remain constant (2/3) ensuring that a constant fraction 1/3 is always delivered to the distal nephron where its salt content can be regulated.

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20
Q

When is renal insterstitial hydrostatic pressure increased?

A

When there is a lower GFR

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21
Q

When ECV is low (thus GFR is reduced) what happens to reabsorption of salt and water at PCT and why?

A

Increase in peritubular capillary hydrostatic pressure. Decrease in colloid osmotic pressure (due to a decreased filtration)

Increased renal interstitial volume and/or pressure (due do lower GFR), raises the permeability of the tight junctional complexes of the proximal tubule. Increases the back leak of sodium from the interstitium into the tubule lumen.
Reduction of sodium and water reabsorption across the proximal tubule, more water and salt moves onto distal nephron where It can be regulated .

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22
Q

When ECV is high (thus GFR is increased) what happens to reabsorption of salt and water at PCT and why?

A

Decreases in peritubular capillary hydrostatic pressure and increases in colloid osmotic pressure

Decrease in RIHP would reduce back leak of sodium from the interstitium and enhance proximal tubule sodium reabsorption.

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23
Q

Why is it beneficial that when ECV is low we reabsorb less Na+ at the PCT?

A

To maintain the constant proportion (1/3) of filtrate that reaches the distal nephron for effective regulation

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24
Q

Where are renins effects on the kidney tubule mainly?

A

After the macula densa

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25
Q

Why does low Na+ in the MD stimulate increased Na+ absorption?

A

Low Na+ in MD is a proxy for low GFR (less fluid reaching the DCT)

Aldosterone increases Na+ absorption at CD to increase blood osmolarity

26
Q

How does an increase in medullary blood flow affect Na+ reabsorption?

A

Leads to a washout of medullary interstitial hypertonicity.

Less water abstraction out of the thin descending limb

Reduced sodium concentration decreases so less sodium reabsorption, and more sodium is excreted.

27
Q

How does raised concentration of NaCl at the MD inhibit renin release and decrease GFR?

A

Na-K-2Cl cotransporters (NKCC2), on macula densa cells, pump more sodium into the cells.

Increases the cell’s osmolarity (not enough Na/KATPase)

Water flows along the osmotic gradient, causing the cell to swell.

When the cell swells, ATP escapes through a basolateral, stretch-activated, non-selective ion channel.

ATP converted to adenosine by ecto-5′-nucleotidase.

Adenosine constricts the afferent arteriole by binding to the A1 receptors. Adenosine binds to A2 receptors causing dilation of efferent arterioles.

Afferent constriction decreases the glomerular filtrate rate.

Decrease in cAMP inhibits Renin release from the juxtaglomerular cells.

28
Q

How does lowered concentration of NaCl at the MD promote renin release?

A

NKCC2 has a lower activity and subsequently causes a complicated signaling cascade

This causes the synthesis and release of PGE2.

PGE2 acts on EP2 and EP4 receptors in juxtaglomerular cells and causes renin release.

Renin release activates RAAS leading to many outcomes including an increased GFR.

29
Q

What 4 effects does ADH release have?

A

Causing insertion of AQP2 into the apical membrane of principle CD cells (increase water reabsorption)

Stimulates the NKCC channel more water reabsorption in CD

Urea transporter is upregulated

Slows the blood flow in the vasa recta to reduce depletion of medullary solutes by blood flow.

30
Q

How does the sympathetic nervous system reduce Na+ excretion?

A

Renal nerves act directly on the tubule to increase sodium reabsorption via an a-adrenergic receptor.

Increases in renal sympathetic nerve activity activates the renin angiotensin system.

Raise renal vascular resistance: Decrease GFR, medullary blood flow, and renal interstitial pressure.

31
Q

What happens in juxtoglomerular cells when renin secretion stimulated?

A

Precursor pro-renin is converted to renin then secreted

32
Q

What organ releases angiotensinogen?

A

Liver

33
Q

What happens to plasma renin?

A

Converts angiotensinogen to angiotensin I

34
Q

Where is angiotensin converting enzyme found?

A

On the surface of vascular endothelial cells, predominantly those of the lungs.

35
Q

What happens to angiotensin I?

A

Converted to angiotensin II by angiotensin converting enzyme

36
Q

What effects does angiotensin II have (5)?

A

Stimulates aldosterone release from adrenal cortex

Renal vasoconstriction efferent more than afferent

Enhanced proximal tubule reabsorption. (Na+/H+)

Heightened sensitivity of macula densa to distal flow rate

Stimulated thirst, ADH release

Vasoconstriction

37
Q

What does efferent vasoconstriction cause?

A

Increase in GFR, lowered hydrostatic pressure in peritubular capillaries and elevated oncotic pressure (overall more Na+ uptake into the blood and reduced back-flux)

38
Q

What type of hormone is aldosterone?

A

Steroid

39
Q

Where is aldosterone released from?

A

Adrenal cortex

40
Q

Where does aldosterone bind?

A

Nuclear mineralocorticoid receptors (MR) within the principal cells of the distal tubule and the collecting duct of the kidney nephron

41
Q

What does aldosterone do?

A

Upregulates and activates the basolateral Na+/K+ pump and apical Na+ transporters (ENaC).

This results in more reabsorption of sodium (Na+) ions and water (which follows sodium) into the blood,

42
Q

Why is aldosterone release stimulated by increased plasma potassium?

A

Secretes potassium (K+) ions into the urine (lumen of collecting duct)

43
Q

Why is Cl− reabsorbed in conjunction with sodium cations?

A

To maintain the system’s electrochemical balance.

44
Q

What antagonises aldosterone receptor?

A

Spironolactone

45
Q

How does aldosterone enhance proximal tubule reabsorption?

A

Stimulates the Na+/H+ exchanger to increase its activity.

More Na+ is bought in apically, leading to more Na+ absorption in addition to control by starling forces.

46
Q

Where is ANP synthesised?

A

Atrial myocytes

47
Q

Under what circumstances is ANP released?

A

Increased atrial distention

48
Q

How does ANP increase Na+ excretion?

A

Increasing GFR and reducing sodium reabsorption

49
Q

How does ANP inhibit Na+ reabsorption directly?

A

Directly inhibits sodium reabsorption in the collecting duct via a cGMP-mediated reduction in sodium permeability.

50
Q

How does ANP inhibit Na+ reabsorption indirectly?

A

Indirectly by increasing medullary blood flow (vasodilation) and inhibiting the formation of ANG II and aldosterone.

51
Q

How does ADH affect renin release?

A

Inhibits it (-ve feedback)

52
Q

What channel does ADH cause insertion into CD?

A

AQPII

53
Q

How does renin affect ADH release?

A

Stimulates it

54
Q

What secondary messenger mediates the action of ANP?

A

cGMP

55
Q

What effect does V2 receptor occupancy have?

A

Increases cAMP

PKA phosphorylates cytoskeletal elements associated with vesicles that contain AQP2 channels.

Causes the exocytosis of these vesicles and thus the merging of AQP2 with the apical membrane

56
Q

When Na+ delivery is high to MD, tubuloglomerular feedback results in

A

Afferent arteriole constriction, decreased renin release

57
Q

What is the critical target of the JGA signaling cascade?

A

Glomerular afferent arteriole

58
Q

When Na+ delivery is low to MD, tubuloglomerular feedback results in

A

Afferent arteriole dilation (prostaglandin release), Renin release

59
Q

Is the vasa recta supplied by the afferent arteriole?

A

No

60
Q

How is GFR modified through widespread regulation?

A

Renin release - angiotensin II - efferent arteriole constriction increases GFR

vice versa

61
Q

Strong activation of renal sympathetic nerves…

A

decreases GFR

62
Q

Tubuloglomerular feedback results in

A

Afferent arteriole contraction + decreased renin release / afferent arteriole relaxation + increased renin release

Kidney physiology (7 decks)

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