Sodium And Potassium Balance

Question 1

What is the most prevalent solute in ECF?

Answer 1

Sodium

Question 2

How does an increase in Sodium diet affect blood pressure and volume?

Answer 2

It increases ECF sodium = increased water retained and therefore ECF = increased blood pressure and volume

Question 3

What 2 mechanisms are in place to increase or decrease appetite for sodium?

Answer 3

Centrally there is the Latéral parabrachial nucleus which make you crave salt depending on the sodium levels in the ECF
Taste buds like sodium taste until there is too much where it no longer tastes nice

Question 4

How much sodium is absorbed in each part of the nephron?
What is the relationship between the distal convoluted tubule and the glomerulus?

Answer 4

67% in PCT
25% in thick ascending limb
5% in DCT
3% in collecting duct
They are close by, so that if there Is an increase in Na+ in the DCT (due to increased GFR) adenosine can be released from the macula densa cells on the DCT to be detected by extraglomerular mesangial cells, this causes the below=
decreased amount of renin produced (no angiotensin = less aldosterone = less salt retention)
Causes smooth muscle cells to contract on afférent arteriole
Reduced perfusion pressure and GFR

Question 5

How do we retain sodium?

Answer 5

Sympathetic activity stimulation
Causes less filtration of Na+
Stimulâtes afférent arteriole smooth muscle to contract
Stimulates na+ uptake of PCT
Stimulates juxtaglomerular cells to produce renin
Renin = angiotensin II = PCT further stimulated to take up NA+
Angiontensin II also stimulates aldosterone release = more Na+ uptake by DCT and CD

Question 6

How do we decrease sodium?

Answer 6

Via atrial natriuretic peptide
Decreases afférent arteriole contraction
Inhibits PCT
Inhibits renin secretion
Decreases Na+ uptake of DCT and CT

Question 7

What happens to our blood pressure, fluid volume, activity of B1-sympathetic and renin (therefore aldosterone and vasoconstriction) in states of low and high sodium?

Answer 7

Low Na+= low BP, low fluid volume, increased B1 activity, increased renin = increased aldosterone and increased vasoconstriction
High sodium = opposite

Question 8

How is aldosterone synthesised?
What two factors drive its synthesis?
What is its function on a cellular level?
What can excess levels lead to?

Answer 8

Made in zoma glomerulosa in adrenal cortex
Released in response to angiotensin II and a decrease in BP via baroreceptors

Stimulates Na+ réabsorption by activating na channels on DCT
Stimulates Potassium secretion
Increased hydrogen ion secretion

Can lead to alkalaemic alkalosis if in excess of aldosterone

Question 9

How does aldosterone work on the cell?

Answer 9

Binds to mineralcorticoid receptor on the cell
Binds to nucleus dna = RNA = transcription

Question 10

What molecules does aldosterone have a negative feedback loop effect on?
How does hypoaldosteronism present?
How does hyperaldosteronism present?

Answer 10

Renin
Ang II
ADH

Dizziness, low BP, salt cravings, palpitations
High BP, thirst, polyuria

Question 11

What is Liddle’s syndrome?

Answer 11

Inherited Mutation in aldosterone activated sodium channel on lumen side
Channel is always ‘on’
Results in sodium retention and increased BP

Question 12

What do baroreceptors do?
How is blood pressure detected on the low pressure and high pressure side of the cardiovascular system?

Answer 12

Measure BP
Low pressure side can detect high and low blood pressure
Low BP: reduced baroreceptor firing = afférent fibres go to brain stem causing an increase in ADH and sympathetic activity
High BP: increased atrial stretch releases ANP and BNP

High pressure side can only detect low blood pressure
Low BP: reduced baroreceptor firing: JGA cells decrease renin secretion and afférent fibres go to brainstem to release ADH and increase sympathetic activity

Question 13

What do ANP and BNP do?
Where are they made?

Answer 13

Small peptides made in atria which are released in response to atrial stretch (eg high BP)
Cause vasodilation of renal blood vessels
Inhibition of sodium reuptake in PCT and CD
Inhibits release of renin and aldosterone
Reduces blood pressure

Question 14

How does an increase in Na+ in the CT affect the amount of water reabsorped?

Answer 14

Reduces amount of water reabsorbed as there is a decrease in osmotic gradient between the CT and the lumen

Question 15

What are the effects of ACE inhibitors?

Answer 15

Inhibits angiotensin II production
= decrease Na+ reuptake in PCT
Increase of na+ amount that reaches CD = decreased water reabosprtion (due decreased osmolar difference)
Causes vasodilation
Reduces aldosterone release indirectly
= reduced blood pressure

Question 16

What is the instant response to increase dietary K+?

Answer 16

Insulin activates the Na/H+ exchanger on cells
The increased levels of intracellular Na+ activates the Na/K+/ATP pump = increased K+ intracellular from the plasma and decreased Na+ (back into ECF)

Question 17

What are the causes of hypokalaemia?

Answer 17

Too much processed food
Diuretics
Vomiting
Diarrhoea

Question 18

What causes hyperkalaemia?

Answer 18

K+ sparing diuretics
ACE inhibitors
Elderly
Severe diabetes
Kidney disease

Question 19

What are the diuretics available and what part of the nephron do they act on?

Answer 19

Osmotic diuretics: act on the proximal convoluted tubules to reabsorbed less water
Carbonic anhydrase inhibitors: on the proximal convoluted tubules
Loop diuretics: thick ascending limb
Thiazide diuretics: DCT
K+ sparing diuretics on collecting duct

Question 20

How do carbonic anhydrase inhibitors work?

Answer 20

They inhibit carbonic anhydrase which turns H2C03 into H20 and C02 in the tubular lumen
This C02 would’ve come back into the cell, and be turned into H2C03 again and therefore made H+ and HC03+
This H+ would have gone through an sodium transporter back out into the lumen, and allowed sodium reuptake into the cell
None of this is possible without carbonic anhydrase activity

Question 21

How do loop diuretics work?

Answer 21

They block the sodium,potassium chloride triple transporter on the luminal side
This means that less na+ Is reuptaked
It also means that more na+ will be in the lumen at the collecting duct area increasing the osmolar gradient = more water réabsorption

Question 22

How do thiazides work?
What other molecule doe they also cause a réabsorption in?

Answer 22

Block the Na+/Cl- transporter
Also increase calcium réabsorption

Question 23

How do potassium sparing diuretics work?

Answer 23

They inhibit aldosterone function
Therefore less sodium channels are activated on the CD

Question 24

What levels of potassium are excreted/reabsorbed in each nephron parts?

Answer 24

PCT: 67%
TAL: 20%
DCT: 10-50% excreted
CD: 5-30% excreted