kidney function III: regulation of ECF and blood volume Flashcards

1
Q

What are some causes of increased extracellular fluid (ECF) osmolality?

A

Water deprivation, solute ingestion, diarrhea.

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2
Q

What happens when ECF osmolality increases?

A

Osmoreceptors detect the change and initiate responses.

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3
Q

What are the two key osmoreceptor areas in the brain?

A

Supraoptic & paraventricular nuclei

Lateral preoptic area

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4
Q

What is the function of the supraoptic & paraventricular nuclei?

A

They stimulate ADH release from the posterior pituitary.

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5
Q

What does ADH do after being released from the posterior pituitary?

A

It makes the collecting duct (CD) water-permeable, leading to water retention by the kidneys.

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6
Q

What is the function of the lateral preoptic area?

A

It stimulates thirst, prompting the person to drink water.

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7
Q

How does drinking water and water retention restore balance?

A

It reduces ECF osmolality, bringing it back to normal (290 mosm/kg).

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8
Q

what process happen in water excretion instead?

A

opposite of water retention

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9
Q

What can cause a decrease in extracellular fluid (ECF) osmolality?

A

Excessive fluid ingestion.

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10
Q

What happens when ECF osmolality decreases?

A

Osmoreceptors detect the change and initiate responses.

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11
Q

What are the two key osmoreceptor areas in the brain?

A

supraoptic & paraventricular nuclei

Lateral preoptic area

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12
Q

What happens when the supraoptic & paraventricular nuclei detect low osmolality?

A

ADH release is suppressed, making the collecting duct (CD) water-impermeable.

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13
Q

What is the function of the lateral preoptic area in response to low osmolality?

A

It suppresses thirst, reducing fluid intake.

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14
Q

How does the kidney respond to suppressed ADH?

A

It excretes more water, restoring osmolality to normal (290 mosm/kg).

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15
Q

What is osmolality?

A

The concentration of water in the extracellular fluid (ECF), which is tightly controlled.

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16
Q

What determines the volume of the extracellular fluid (ECF)?

A

The total quantity of solute, mainly NaCl (sodium chloride)

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17
Q

What is the key factor in ECF volume regulation?

A

Sodium balance.

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18
Q

How much dietary salt (NaCl) is typically consumed per day?

A

It varies between 0.05g to 25g per day, with an average of 2.3g/day.

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19
Q

What dictates the volume of the extracellular fluid (ECF)?

A

The total amount of sodium (NaCl) in the ECF.

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20
Q

What happens when 0.2g NaCl is added to 1L of water?

A

The concentration increases from 1g/L to 1.2g/L.

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21
Q

How does osmoregulation correct changes in ECF osmolality?

A

It increases water retention, diluting the concentration back to 1g/L.

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22
Q

What is the final volume after osmoregulation when 1.2g NaCl is present?

A

1.2L of water is retained to restore normal concentration.

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23
Q

What are the major compartments of body water?

A

Intracellular water (28L)

Extracellular fluid (ECF) – includes:
Interstitial water (10L)
Plasma (4L)

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24
Q

What are the key solutes in body fluids?

A

Sodium (Na⁺) – Mostly in ECF

Potassium (K⁺) – Mostly in intracellular fluid

Glucose – Found in small amounts

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25
Q

Why is plasma volume important?

A

It determines blood pressure in veins, cardiac chambers, and arteries.

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26
Q

What happens if total body sodium is low?

A

Low plasma volume
Low cardiovascular pressures

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27
Q

What does the body directly control in the vascular system?

A

The osmolality and volume of the extracellular fluid (ECF).

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28
Q

How does the control of ECF osmolality and volume affect the body?

A

It affects the osmolality and volume of other compartments in the body.

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29
Q

How is ECF osmolality normally maintained?

A

At the expense of volume.

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30
Q

What controls water balance (H₂O) in the body?

A

osmoreceptors.

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31
Q

How do osmoreceptors regulate water balance?

A

Renal excretion by altering ADH release.

Water intake by altering thirst.

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32
Q

How is sodium excretion in urine determined?

A

Sodium excreted in urine = Sodium filtered - Sodium reabsorbed.

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33
Q

What are the two main factors that regulate sodium (Na⁺) content in the body?

A

Glomerular Filtration Rate (GFR)

Sodium Reabsorption

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34
Q

Is there strong evidence for a regulatory “Na⁺ appetite” in humans?

A

No, there is little evidence for a regulated sodium appetite in humans.

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35
Q

What does glomerular filtration rate (GFR) depend on?

A

Net filtration pressure

Permeability of filtration interface

Surface area

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36
Q

How is GFR regulated?

A

By both neural and hormonal input.

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37
Q

What does a higher GFR result in?

A

Greater excretion of salt and water.

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38
Q

What is Intrinsic Control of GFR?

A

Internal to the kidney, it protects renal capillaries from hypertensive damage and maintains a healthy GFR.

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39
Q

What is Extrinsic Control of GFR?

A

External to the kidney, it maintains arterial blood pressure by controlling GFR.

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40
Q

What is the Intrinsic Control of GFR?

A

It protects renal capillaries from hypertensive damage and maintains a healthy GFR.

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41
Q

How does Intrinsic Control regulate GFR when blood pressure changes?

A

Afferent arterioles constrict when BP suddenly increases.

Afferent arterioles dilate when BP suddenly decreases.

This keeps capillary pressure and glomerular blood flow constant.

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42
Q

What is the normal BP range where Intrinsic Control maintains GFR?

A

Between 90-200 mmHg.

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43
Q

What is Autoregulation in GFR control?

A

The kidney’s ability to maintain constant renal blood flow despite changes in BP.

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44
Q

What is Autoregulation in the kidney?

A

The ability to control afferent arteriole constriction to regulate glomerular filtration rate (GFR).

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45
Q

What are the mechanisms of autoregulation in the kidney?

A

Myogenic response
Tubuloglomerular feedback

46
Q

What is the myogenic response in renal autoregulation?

A

A mechanism where afferent arterioles constrict in response to increased blood pressure, helping maintain constant glomerular filtration rate (GFR).

47
Q

What happens to smooth muscle cells in response to increased hydrostatic pressure?

A

Stretch-activated calcium channels open
Smooth muscle contracts
Afferent arteriole vasoconstricts
GFR remains stable

48
Q

How does the myogenic response regulate renal blood flow?

A

By adjusting vascular resistance in the afferent arteriole to maintain stable glomerular capillary pressure.

49
Q

what is the tubuloglomerular feedback mechanism?

A

A process where the macula densa detects increased NaCl delivery and signals the afferent arteriole to constrict, reducing glomerular filtration rate (GFR).

50
Q

What happens when NaCl delivery to the macula densa increases?

A
  1. ATP and ADP are released.
  2. Converted to adenosine.
  3. Adenosine binds A1 receptors, increasing Ca²⁺ in vascular smooth muscle cells (VSM).
  4. Vasoconstriction of the afferent arteriole occurs.
  5. GFR decreases to prevent excessive filtration.
51
Q

How does adenosine affect the afferent arteriole?

A

It increases calcium in smooth muscle cells, causing vasoconstriction and a decrease in GFR

52
Q

What is intrinsic control of GFR (autoregulation)?

A

A mechanism where the kidney maintains GFR despite changes in arterial pressure.

53
Q

When is intrinsic control of GFR absent?

A

When arterial pressure falls below 90 mmHg.

54
Q

Why is autoregulation not perfect?

A

Because renal blood flow (RBF) and GFR still fluctuate with arterial pressure.

55
Q

What is extrinsic control of GFR?

A

GFR can be altered by neural and hormonal input when extracellular fluid volume (ECFV) is outside the normal range.

56
Q

Can GFR be controlled by both intrinsic and extrinsic mechanisms?

A

Yes! Intrinsic autoregulation maintains GFR, but extrinsic factors (e.g., hormones, neural signals) can override it.

57
Q

What do sensors regulate in sodium reabsorption?

A

They affect renin or natriuretic peptide secretion.

58
Q

Name the main sensors involved in sodium reabsorption control.

A

Macula densa
Intrarenal baroreceptors (granular juxtaglomerular cells)
High-pressure baroreceptors (central arterial tree)
Low-pressure baroreceptors (cardiopulmonary circuit)
Muscle cells of cardiac atria & ventricles

59
Q

What is the role of renin-angiotensin II-aldosterone in sodium reabsorption?

A

It stimulates Na⁺ reabsorption.

60
Q

How does direct pressure on the kidney affect renin?

A

it stimulates renin release.

61
Q

How do renal sympathetic nerves regulate sodium reabsorption?

A

They stimulate renin release.

62
Q

What is the effect of natriuretic peptides on sodium reabsorption?

A

They cause natriuresis and inhibit Na⁺ reabsorption.

63
Q

What is the juxtaglomerular apparatus (JGA)?

A

A structure in the kidney involved in renin release, consisting of juxtaglomerular cells, macula densa, and extraglomerular mesangial cells.

64
Q

What are the intrinsic mechanisms controlling renin release?

A

Tubuloglomerular feedback
Intrarenal baroreceptors

65
Q

What are the extrinsic mechanisms controlling renin release?

A

Sympathetic nervous system.

66
Q

What is the function of the macula densa?

A

It acts as a sensor that detects NaCl (sodium chloride) levels in the filtrate and regulates renin release.

67
Q

How does increased NaCl delivery to the macula densa affect renin release?

A

Increased NaCl → More adenosine (ADO) formation
Adenosine increases calcium (Ca²⁺) in granular cells
Increased calcium inhibits renin release
Result: Reduced GFR due to afferent arteriole vasoconstriction.

68
Q

What is the key messenger that mediates the macula densa’s effect on renin release?

A

Adenosine (ADO)—it increases calcium in granular juxtaglomerular cells, inhibiting renin release.

69
Q

What is the extrinsic control of renin release?

A

Sympathetic nerves of granular cells receive signals from baroreceptors.

70
Q

What type of nerve fiber is involved in extrinsic control of renin release?

A

Sympathetic nerve fiber.

71
Q

Where are renin-containing cells located?

A

Granular juxtaglomerular cells.

72
Q

What anatomical structure includes juxtaglomerular cells and macula densa?

A

The juxtaglomerular apparatus (JGA).

73
Q

What causes renin release from the kidney?

A

↓ sodium delivery to the macula densa

↓ wall tension in the renal afferent arteriole

↑ sympathetic activity in response to low blood pressure

74
Q

What is a common cause of renin release?

A

Low blood volume (Hypovolemia).

75
Q

What is the precursor molecule in the renin-angiotensin system?

A

Plasma angiotensinogen

76
Q

What enzyme converts angiotensinogen into angiotensin I?

77
Q

What converts angiotensin I into angiotensin II?

A

Plasma ‘converting enzyme’

78
Q

What are the effects of angiotensin II?

A

Stimulates Proximal Tubule Na⁺ Reabsorption
Stimulates ADH Release
Causes Aldosterone Secretion
Causes Thirst
Vasoconstricts Small Arterioles

79
Q

What is the role of Angiotensin II in sodium reabsorption?

A

Angiotensin II stimulates proximal tubule Na⁺ reabsorption by binding to AT1 receptors.

80
Q

What receptor does Angiotensin II bind to for sodium reabsorption?

A

AT1 (Angiotensin II Type 1 receptor).

81
Q

What transporters are involved in sodium reabsorption in the proximal tubule?

A

Na⁺:H⁺ Exchanger (NHE3)
Na⁺:K⁺ ATPase pump

82
Q

Where does Angiotensin II bind in the brain?

A

It binds to angiotensin II receptors in the hypothalamus.

83
Q

What are the two main effects of Angiotensin II binding in the brain?

A

Stimulates ADH release
Causes thirst

84
Q

What brain structure contains osmoreceptors that regulate ADH release?

A

The hypothalamus.

85
Q

What stimulates the release of aldosterone?

A

Angiotensin II stimulates aldosterone release from the adrenal cortex.

86
Q

Where is aldosterone released from?

A

The zona glomerulosa of the adrenal cortex.

87
Q

What is the sequence of events leading to aldosterone release?

A

Renin converts angiotensinogen to angiotensin I.

Angiotensin I is converted to angiotensin II by a converting enzyme.

Angiotensin II stimulates the adrenal cortex to release aldosterone.

88
Q

What is the effect of aldosterone on sodium reabsorption

A

Aldosterone increases Na⁺ reabsorption in the distal convoluted tubule (DCT) and collecting duct (CD).

89
Q

In which parts of the nephron does aldosterone act?

A

Distal convoluted tubule (DCT) and collecting duct (CD).

90
Q

What is the role of renin in the renin-angiotensin system?

A

Renin converts angiotensinogen into angiotensin I.

91
Q

How is angiotensin II formed?

A

Angiotensin I is converted to angiotensin II by a plasma ‘converting enzyme’.

92
Q

What hormone is released by angiotensin II to regulate sodium?

A

Aldosterone is released from the adrenal cortex.

93
Q

What is the effect of aldosterone on sodium?

A

Aldosterone increases sodium reabsorption in the DCT and CD.

94
Q

How does increased sodium reabsorption affect extracellular fluid (ECF)?

A

It leads to ECF expansion via osmoregulation

95
Q

What is the final outcome of this process?

A

Restoration of blood volume and regulation of blood pressure.

96
Q

What is the primary function of aldosterone?

A

Increases sodium (Na⁺) reabsorption in the distal convoluted tubule (DCT) and collecting duct (CD).

98
Q

Aside from the kidney, where else does aldosterone increase Na⁺ reabsorption?

A

Sweat glands, salivary glands, and the gut.

99
Q

How does aldosterone regulate sodium balance?

A

It promotes Na⁺ retention, helping to maintain blood pressure and extracellular fluid volume.

100
Q

What receptor does angiotensin II bind to in renal arterioles?

A

Angiotensin II type 1 (AT1) receptors.

101
Q

How does angiotensin II affect renal arterioles?

A

Vasoconstriction of both afferent and efferent arterioles, reducing GFR.

102
Q

What is the effect of reduced GFR on sodium and water excretion?

A

Decreased sodium and water excretion, helping to conserve blood volume and pressure.

103
Q

What receptor does low plasma angiotensin II bind to in the kidney tubules?

A

Angiotensin II type 2 (AT2) receptors.

104
Q

What renal process is stimulated by low plasma levels of angiotensin II?

A

Pressure natriuresis and diuresis.

105
Q

What triggers the release of natriuretic peptides (NP) in the heart?

A

Heart stretch due to high blood volume.

106
Q

Where is A-type Natriuretic Peptide (ANP) secreted from?

A

Atrial myocardium.

107
Q

Where is B-type Natriuretic Peptide (BNP) secreted from?

A

Ventricular myocardium.

108
Q

What is the natriuretic effect of ANP and BNP?

A

Inhibits Na⁺ entry into collecting duct cells by blocking epithelial sodium channels (ENaC), inhibits renin and aldosterone release.

109
Q

How do ANP and BNP act as diuretics?

A

Inhibit ADH release, reducing water retention.

110
Q

What are the hypotensive effects of ANP and BNP?

A

Decrease blood pressure by systemic vasodilation and increase GFR by dilating renal afferent arterioles.

111
Q

What ion channels are involved in the action of ANP and BNP?