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ESA 3- Urinary System > Changes in Plasma Volume and Renal Control of Blood Pressure > Flashcards

Changes in Plasma Volume and Renal Control of Blood Pressure Flashcards

1
Q

Where is the water in the body located?

A
  • Intracellular fluid (ICF)
  • Extracellular fluid (ECF)
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2
Q

What seperates the intracellular fluid and the extracellular fluid?

A

The cell membrane

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3
Q

What tightly regulates the volumes of the ICF and ECF?

A

Their ionic compositions and osmosis

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4
Q

What is ECF volume determined largely by?

A

The concentration of NaCl

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5
Q

How can the kidney maintain the ECFs volume within a very narrow margin?

A

By regulating the excretion of NaCl

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6
Q

What must the kidneys balance?

A

The amount of Na+ excretion with ingestion

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7
Q

What is the process of matching Na+ secretion with ingestion called?

A

Sodium balance

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8
Q

What is meant by a patient being in positive balance?

A

Na+ excretion is less than intake

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9
Q

What happens when a patient is in positive balance?

A

ECF expansion

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10
Q

Why does a positive sodium balance lead to ECF expansion?

A

Na+ is retained in the body, primarily in the ECF. Water is drawn out of the nephron causing a corresponding increase in volume

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11
Q

What happens as a result of ECF expansion?

With respect to blood volume and arterial pressure

A
  • Blood volume increases
  • Arterial pressure increases

Oedema may follow

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12
Q

What is meant by a patient being in negative balance?

A

Na+ excretion is greater than intake

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13
Q

What happens when a patient is in negative balance?

A

ECF contraction

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14
Q

Why does a negative sodium balance lead to ECF contraction?

A

The Na+ content of the ECF decreases, so less water is drawn out of the nephron, so ECF volume decreases

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15
Q

What happens as a result of ECF contraction?

With respect to blood volume and arterial pressure

A
  • Blood volume decreases
  • Arterial pressure decreases
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16
Q

Do changes in Na+ affect ECF osmolarity?

A

No

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17
Q

Why doesn’t changes in Na+ balance affect ECF osmolarity?

A

If the concentration of Na+ in the ECF increases, then volume increases. The increase in volume gives increased cardiac output, and increased Na+ excretion

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18
Q

What % of Na+ is filtered in the glomerulus?

A

100%

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19
Q

What % of Na+ is reabsorbed in the PCT?

A

67%

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20
Q

What is meant by glomerular tubular balance?

A

The proportion of Na+ reabsorbed is always the same, regardless of the actual amount that is filtered

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21
Q

What does autoregulation do?

A

Prevents GFR from changing too much

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22
Q

What is the result of glomerular tubular balance?

A

If any changes in GFR occur, it blunts out the Na+ excretion response

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23
Q

Is Na+ reabsorption an active or passive process?

A

Mainly active

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24
Q

What drives Na+ reabsorption?

A

3Na-2K-ATPase pumps on the basolateral membrane

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25
Q

What do different segments of the tubule have?

A

Different types of Na+ transporters and channels in the apical membrane

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26
Q

Draw a diagram illustrating the different segments of the tubule that have different types of Na+ transporters and channels

A
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27
Q

What happens in section 1 of the tubule?

A
  • Na+ reabsorption
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28
Q

How does Na+ reabsorption occur in section 1 of the tubule?

A
  • Co-transported with glucose
  • Na-H exchange
  • Co-transport with AA or carboxylic acids
  • Co-transport with phosphate
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29
Q

Other than mechanisms to reabsorb Na+, what does section 1 of the tubule have in its membrane?

A

Aquaporin

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30
Q

What happens to the concentration of urea and Cl- down section 1 of the tubule?

A

It increases

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31
Q

What is the purpose of the increase in Cl- concentration down section 1 of the tubule?

A

It increases the concentration gradient for Cl- reabsorption in sections 2 and 3

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32
Q

Draw a diagram illustrating Na+-Glucose cotransport in section 1 of the tubule

A
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33
Q

What happens in sections 2 and 3 of the tubule?

A
  • Na+ and water reabsorption
  • Cl- reabsorption
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34
Q

How do sections 2 and 3 of the tubule reabsorp Na+?

A

Na-H exchanger

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35
Q

How do sections 2 and 3 of the tubule reabsorb water?

A

Aquaporin

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36
Q

How do sections 2 and 3 of the tubule reabsorb Cl-?

A
  • Paracellular Cl- reabsorption
  • Transcellular Cl- reabsorption
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37
Q

Draw a diagram illustrating the processes that occur in sections 2 and 3 of the tubule

A
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38
Q

What is the overall result of movement of substances in the tubule?

A

It sets up an ~4mOsmol gradient favouring water uptake from the lumen

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39
Q

How water permeable is the PCT?

A

Highly

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40
Q

What does the high water permeability of the PCT allow?

A

Reabsorption to be isosmotic with plasma

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41
Q

What is the reabsorption of water in the PCT driven by?

A
  • Osmotic gradient established by solute reabsorption
  • Hydrostatic force in the intersticium
  • Oncotic force in the peritubular capillary
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42
Q

What produces the oncotic force in the peritubular capillary?

A

The loss of 20% filtrate at the glomerulus, but cells and proteins remained in the blood

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43
Q

Label this graph illustrating how well substances are reabsorbed

A
  • A - Chloride
  • B - Phosphate
  • C - HCO3-
  • Glucose, AA, and lactate
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44
Q

What is meant by glomerulotubular balance?

A

The balance between Glomerular Filtration Rate and the rate of reabsorption of solutes

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45
Q

What must be true of the glomerulotubular balance?

A

It must be kept as constant as possible, so if GFR increases, the rate of reabsorption must also increase

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46
Q

How much Na+ is reabsorbed in the PCT?

A

67%, regardless of GFR

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47
Q

How does an ECF volume increase cause an increase in GFR?

A

If ECF volume increases, cardiac output will increase, causing an increase in arterial blood pressure, which in turn will increase GFR

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48
Q

What happens to the reabsorption of solute and water in the loop of Henle?

A

It is separated

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49
Q

What is reabsorbed in the descending limb?

A

Water, but not NaCl

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50
Q

What is reabsorbed in the ascending limb?

A

NaCl, but not water

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51
Q

What is the ascending limb known as?

A

The diluting segment

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52
Q

Why is the ascending limb known as the diluting segment?

A

Because it dilultes NaCl in the filtrate

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53
Q

How does tubule fluid leaving the loop compared to the plasma?

A

It is hypo-osmotic (more dilute)

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54
Q

Draw a diagram illustrating the seperation of reabsorption in the loop of Henle

A
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55
Q

What does the increase in intracellular concentrations of Na+ set up by the PCT allow for?

A

Paracellular reuptake of water from the descending limb

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56
Q

Are there tight junctions in the descending limb?

A

No

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57
Q

What is the result of the paracellular reuptake of water from the descending limb?

A

It concentrates Na+ and Cl- in the lumen of the descending

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58
Q

Why does Na+ and Cl- need to concentrate in the lumen of the descending limb?

A

Ready for active transport into the ascending

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59
Q

Draw a diagram illustrating reuptake in the descending limb

A
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60
Q

Is the ascending limb permeable to water?

A

No

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61
Q

Why is the ascending limb impermeable to water?

A

Tight junctions

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62
Q

Draw a diagram illustrating uptake in the ascending limb

A
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63
Q

What happens in the thick ascending limb (TAL)?

A
  • NaCl is transported from the lumen into cells by NaKCC2 channel
  • Na+ then moves into the intersticium due to the action of 3Na-2K-ATPase
  • K+ ions diffuse back into the lumen via ROMK
  • Cl- ions move into the Intersticium
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64
Q

What is NaKCC2 a target of?

A

Loop diuretics

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65
Q

What does increased loss of K+ in the urine lead to?

A

Hypokalaemia

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66
Q

How does the energy use of the thick ascending limb differ from other regions of the nephron?

A

It is much higher

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67
Q

What is the TAL particularly sensitive too?

A

Hypoxia

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68
Q

Draw a diagram illustrating what happens in the TAL

A
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69
Q

How water permeable is the DCT?

A

Fairly low

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70
Q

What does the active reabsorption of Na+ in the DCT result in?

A

Dilution of the filtrate

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71
Q

What enters the distal convoluted tubule from the loop of Henle?

A

Hypo-osmotic fluid

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72
Q

What happens to the hypo-osmotic fluid in the distal convoluted tubule?

A

5-8% of its Na+ is actively transported

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73
Q

How is Na+ actively transported in the DCT?

A

NaCC

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74
Q

What drives NaCC?

A

3Na-2K-ATPase

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75
Q

What is the NCC transporter sensitive too?

A

Thiazide diuretics

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76
Q

What is the DCT a major site of?

A

Calcium reabsorption via PTH

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77
Q

What is the result of dilution in the DCT?

A

The fluid that leaves is more hypo-osmotic

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78
Q

Draw a diagram illustrating what happens in the DCT

A
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79
Q

What is the collecting duct?

A

The region responsible for fine-tuning the filtrate

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80
Q

What is the collecting duct able to do?

A

Respond to a variety of stimulants

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81
Q

What are the distinct cell types of the collecting duct?

A
  • Principal cells
  • Intercalated cells
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82
Q

What % of CD cells are principal cells?

A

70%

83
Q

What is the function of principal cells in the CD?

A
  • Reabsorb Na+
  • Produces lumen charge
  • Variable water uptake
84
Q

How is Na+ reabsorbed in principal cells?

A

Epithelial Na+ Channel (ENaC)

85
Q

What drives ENaC?

A

3Na-2K-ATPase

86
Q

What is the importance of the lumen charge produced by principal cells?

A

Electrical gradient for paracellular Cl- reabsorption

87
Q

How do principal cells produce the lumen charge?

A

Potassium secretion into the lumen

88
Q

How do principal cells take up water?

A

Aquaporin 2

89
Q

What is aquaporin 2 dependent on?

A

ADH

90
Q

How do principal cells differ from intercalated cells?

A

They have a more distinct membrane

91
Q

Draw a diagram illustrating what happens in intercalated cells

A
92
Q

What is the function of intercalated cells?

A
  • Active reabsorption of Chloride
  • Secrete H+ ions or HCO3-
93
Q

What is this histograph showing

A

Collecting ducts

94
Q

Label this histograph

A
  • A - Intercalated cells
  • B - Basement membrane
95
Q

How many neurohormonal factors control blood pressure?

A

4

96
Q

How do the neurohormonal factors controlling blood pressure all work in part?

A

By controlling sodium balance and ECF volume

97
Q

What effect does increased Na+ reabsorption have on BP?

A

Increases it

98
Q

What are the neurohormonal factors controlling blood pressure?

A
  • Renin-angiotensin-aldosterone system
  • Sympathetic nervous system
  • Antidiuretic hormone
  • Arial Natriuretic peptide
99
Q

Via what does the sympathetic nervous system exert an effect on blood pressure

A
  • α1-adrenoceptors
  • ß1-adrenoceptors
100
Q

How do α1-adrenoceptors exert an effect on blood pressure?

A

By causing vasoconstriction

101
Q

How do ß1-adrenoceptors exert an effect on blood pressure?

A

It increases the force/rate on heart contraction

102
Q

What effect does the sympathetic nervous system have on renal blood flow?

A

Decreases it

103
Q

What is the result of decreased renal blood flow?

A
  • Decreased GFR and Na+ excretion
  • Activates Na/H exchanger in PCT
104
Q

What effect does the sympathetic nervous system have on renin?

A

It stimulates its release from juxtaglomerular cells

105
Q

What is the result of sympathetic nervous system stimulated renin release?

A

Increased Angiotensin II and aldosterone levels

106
Q

How does the action of arial natiuretic peptide (ANP) differ from the other neurohormonal factors controlling blood pressure?

A

It works in the opposite direction

107
Q

Where is ANP synthesised?

A

Atrial myocytes

108
Q

Where is ANP stored?

A

Atrial myocytes

109
Q

What does ANP promote?

A

Na+ excretion

110
Q

What is the result of Na+ secretion caused by ANP?

A

Causes vasodilation of afferent arteriole

111
Q

How does ANP control blood pressure?

A
  • When there is a high BP;
    1. Atrial cells are stretched
    2. This leads to increased ANP release
    3. This leads to increased Na+ excretion
    4. Volume decreases
    5. BP decreases
  • When there is a low BP;
    1. Atrial cells are less stretched
    2. Reduced ANP release
    3. Volume increases
    4. BP increases
112
Q

What is the action of ANP?

A

Inhibits Na+ reabsorption along the nephron

113
Q

What detects reduced perfusion pressure in the kidney?

A

Baroreceptors in the afferent arteriole

114
Q

What does reduced perfusion pressure in the kidney cause?

A

The release of renin from the granular cells of the juxtagomerular apparatus

115
Q

What causes sympathetic stimulation to the JGA?

A

Decreased NaCl concentration at the Macula Densa cells

116
Q

What would cause decreased NaCl concentration at the Macula Densa cells?

A

Due to low perfusion and therefore low GFR

117
Q

What does sympathetic stimulation to the JGA do?

A

Increase the release of renin

118
Q

Other than sympathetic stimulation, what does decreased NaCl concentration at the Macula Densa cells cause?

A

The Macula Densa cells to release prostaglandins, and so cause afferent vasodilation

119
Q

Label this diagram and show how it relates to the regulation of blood pressure

A
  • A - Afferent arteriole
  • B - Granular cells or juxtaglomerular cells
  • C - Distal tubule
  • D - Macula densa
  • E - Efferent arteriole
  • F - Glomerular capillaries
  • G - Proximal tubule
  • H - Intraglomerular mesangial cells
  • I - Bowman’s space
  • J - Podocyte
  • K - Extraglomerular mesangial cells
  1. Decreased NaCl concentration at the macula densa
  2. Sympathetic stimulation to juxtaglomerular appartus
  3. Decreased renal perfusion pressure (sensed by renal baroreceptors)
120
Q

What does renin do?

A

Cleaves angiotensinogen to angiotensin I

121
Q

What happens to angiotensin I?

A

It is cleaved to form the active hormone Angiotensin II

122
Q

What cleaves angiotensin I to angiotensin II?

A

Angiotensin converting enzyme (ACE)

123
Q

Draw a diagram illustrating the renin-angiotensin system

A
124
Q

What are the types of angiotensin II receptors?

A
  • AT1
  • AT2
125
Q

What kind of receptors are the angiotensin II receptors?

A

G-protein coupled receptors

126
Q

What receptor is the main action of angiotensin II via?

A

The AT1 receptor

127
Q

What sites does angiotensin II act at?

A
  • Arterioles
  • Kidney
  • Sympathetic NS
  • Adrenal cortex
  • Hypothalamus
128
Q

What is the action of angiotensin II at the arterioles?

A

Vasoconstriction

129
Q

What is the action of angiotensin II at the kidney?

A

Stimulates Na+ reabsorption at the kidney

130
Q

What is the action of angiotensin II on the sympathetic nervous system?

A

Increased release of NA

131
Q

What is the action of angiotensin II at the adrenal cortex?

A

Stimulates release of aldosterone

132
Q

What is the action of angiotensin II on the hypothalamus?

A

Increases thirst sensation

133
Q

How does angiotensin II increase thirst sensation?

A

Stimulates ADH release

134
Q

What are the actions of angiotensin II?

A
  • Vasoconstriction
  • Aldosterone release
  • Sympathetic activity
  • Increased Na+ reabsorption
  • Thirst
  • Breaks down bradykinin
135
Q

In what cells does angiotensin II cause vasoconstriction?

A

Vascular smooth muscle

136
Q

What is the effect of angiotensin II induced vasoconstriction?

A

Increasess TPR and therefore BP

137
Q

Where does angiotensin II cause vasoconstriction?

A

In the afferent and efferent arteriole

138
Q

How does angiotensin II stimulate the release of aldosterone?

A

It stimulates the adrenal cortex to synthesise and release aldosterone

139
Q

What does aldosterone do?

A
  • Stimulates Na+ and therefore water reabsorption
  • Activates ENaC and apical K+ channels
  • Increases basolateral Na+ extrusion
140
Q

How does aldosterone increase basolateral Na+ extrusion?

A

Via 3Na-2K-ATPase

141
Q

What does aldosterone act on?

A

Principal cells of CD

142
Q

How does aldosterone increase Na+ reabsorption?

A

Stimulates Na-H exchanger in the apical membrane of PCT

143
Q

What is bradykinin?

A

A vasodilatory

144
Q

Draw a diagram illustrating the action of aldosterone

A
145
Q

What does the baroreceptor reflex work to do?

A

Control acute changes in BP

146
Q

On what time scale does the baroreceptor reflex work?

A

Produces a rapid response, but does not control sustained increases

147
Q

Why does the baroreceptor reflex not control sustained increases in blood pressure?

A

As the threshold for baroreceptor firing resets

148
Q

What does a 5-10% drop in blood pressure cause?

A

Low-pressure baroreceptors in the atria and pulmonary vasculature to send signals to the brainstem

149
Q

How do low-pressure baroreceptors in the atria and pulmonary vasculature sendd signals to the brainstem?

A

Via the vagus nerve

150
Q

What do the signals sent to the brainstem from the low-pressure baroreceptors in the atria and pulmonary vasculature do?

A

Modulate both sympathetic nerve outflow, secretion of the hormone ADH, and reduction of ANP release

151
Q

What does a 5-150% change in blood pressure cause?

A

High-pressure baroreceptors to send impulses

152
Q

Where are high-pressure baroreceptors located?

A

In the carotid sinus and aortic arch

153
Q

What do high-pressure baroreceptors send impulses via?

A

The vagus and glossopharyngeal nerves

154
Q

What is the effect of a decrease in blood pressure?

A
  • Increase sympathetic nerve activity
  • Increase secretion of ADH
155
Q

What are the actions of ADH?

A
  • Addition of aquaporin to the collecting duct
  • Stimulates apical Na/K/Cl co-transporter
156
Q

What is the purpose of the addition of aquaporin to the collecting duct?

A

Allows the reabsorption of water

157
Q

What is the result of the reabsorption of water through aquaporin?

A

It forms concentrated urine

158
Q

What is the release of ADH stimulated by?

A
  • Increases in plasma osmolarity
  • Severe hypovolemia
159
Q

Where does ADH stimulate the apical Na/K/Cl co-transporter?

A

In the thick ascending limb

160
Q

What is the result of ADH stimulation of apical Na/K/Cl co-transporter?

A

Less Na+ moves out into the medulla

161
Q

What is the result of less Na+ moving out into the medulla?

A

Reduces the osmotic gradient for water to exit the lumen into the peritubular capillaries from the thin descending limb

162
Q

What are prostaglandins?

A

Vasodilators

163
Q

What do locally acting prostaglandins do?

A
  • Enhance glomerular filtration
  • Reduce Na+ reabsorption
164
Q

What is the main locally acting prostaglandin?

A

PGE2

165
Q

What important protective function do prostaglandins have?

A

Act as a buffer to excessive vasoconstriction by the sympathetic nervous system and the RAAS

166
Q

What do non-steroidal anti-inflammatory drugs (NSAIDs) do?

A

Inhibit the cyclo-oxygenase (COX) pathway

167
Q

What is the COX pathway involved in?

A

The formation of prostaglandins

168
Q

When should NSAIDs not be administered?

A

When renal perfusion is compromised

169
Q

Give an example of when renal perfusion may be compromised

A

In renal disease

170
Q

Why should NSAIDs not be administed when renal perfusion is compromised?

A

As prostaglandins help maintain renal blood flow and GFR in the presence of vasoconstrictors, if NSAIDs are administered, the GFR is further decreased, leading to acute renal failure

171
Q

What can happen if NSAIDs are given to patients in heart failure or with hypertension?

A

They can exacerbate the condition

172
Q

Why can NSAIDs exacerbate heart failure or hypertension?

A

Because they can increase NaCl and water retention

173
Q

What is hypertension?

A

A sustained increase in blood pressure

174
Q

What is essential hypertension?

A

Hypertension when the cause is unknown

175
Q

What % of hypertension cases are essential hypertension?

A

95%

176
Q

What factors may be involved in essential hypertension?

A
  • Genetic
  • Environmental
177
Q

What is secondary hypertension?

A

Hypertension where a cause can be defined

178
Q

What is important in secondary hypertension?

A

To treat the primary cause

179
Q

Give 4 diseases that can give rise to secondary hypertension

A
  • Renovascular disease
  • Chronic renal diseease
  • Aldosteronism
  • Cushing’s syndrome
180
Q

What is classified as mild hypertension?

A

140-159mmHg systolic/90-99mmHg diastolic

181
Q

What is classified as moderate hypertension?

A

160-179mmHg systolic/100-109mmHg diastolic

182
Q

What is classified as severe hypertension?

A

>180mmHg systolic/>110mmHg diastolic

183
Q

What is renovascular disease caused by?

A

An occlusion of the renal artery

184
Q

What does an occlusion of the renal artery cause?

A

A fall in perfusion pressure in that kidney

185
Q

What does decreased perfusion of the kidney lead to?

A
  • That kidney releasing renin and activating RAAS
  • Vasoconstriction and Na+ retention will then take place at the other kidney
186
Q

What are the adrenal causes of hypertension?

A
  • Conn’s Syndrome
  • Cushing’s Syndrome
  • Pheochromocytoma
187
Q

What is Conn’s Syndrome?

A

An aldosterone secreting adenoma

188
Q

What does Conn’s syndrome cause?

A

Hypertension and hypokalaemia

189
Q

What is Cushing’s syndrome?

A

Excess cortisol

190
Q

How does Cushing’s syndrome cause hypertension?

A

At high concentrations, cortisol acts on aldosterone receptors, causing Na+ and water retention

191
Q

What is a pheochromocytoma?

A

Tumour of the adrenal medulla

192
Q

What does a pheochromocytoma secrete?

A
  • Noradrenaline
  • Adrenaline
193
Q

How is hypertension treated?

A
  • ACE inhibitors
  • Thiazide Diuretics
  • Vasodilators
  • Beta blockers
194
Q

What are ACE inhibitors?

A

Angiotensin II receptor antagonists

195
Q

What is ACE inhibitors mechanism of action?

A

They prevent the production of Angiotensin II from Angiotensin I

196
Q

What do thiazide diuretics do?

A

Inhibit NaCC co-transporter on apical membrane of DCT

197
Q

What may thiazide diuretics cause?

A

Hypokalaemia

198
Q

Why may thiazide diuretics cause hypokalaemia?

A

More K+ lost in urine

199
Q

What are the types of vasodilators used in the treatment of hypertension?

A
  • Ca2+ channel blockers
  • α1 channel blockers
200
Q

What do Ca2+ channel blocks do?

A

Reduce Ca2+ entry into smooth muscle cells

201
Q

What do α1 receptor blockers do?

A

Reduce sympathetic tone

202
Q

What do beta blockers act on?

A

ß1-receptors in the heart

203
Q

What do beta blockers do?

A

Reduce heart rate and contractility

204
Q

What are the non-pharmacological approaches to the treatment of hypertension?

A
  • Diet
  • Exercise
  • Reduced sodium intake
  • Reduced alcohol intake

ESA 3- Urinary System (13 decks)

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