Sodium and Potassium Balance

Question 1

State the relative amounts of sodium reabsorbed in different parts of the nephron.

Answer 1

65% - PCT
25% - loop of Henle
8% - DCT
Up to 2% - collecting duct

Question 2

Describe the relationship between GFR and sodium reabsorption.

Answer 2

The greater the GFR the greater the sodium reabsorption

Question 3

How can you alter GFR to preserve sodium? What components are involved in the preservation of sodium?

Answer 3

Reduce the amount of blood going through the kidneys
Aldosterone - stimulates reabsorption of sodium from the DCT and collecting duct
Angiotensin II - stimulates reabsorption of sodium from the PCT (and stimulates release of aldosterone)
Increased sympathetic activity causes vasoconstriction of the afferent arteriole so less blood reaches the nephron. It also stimulates the JGA and PCT to reabsorb more Na+.
JGA is also stimulated by low tubular Na+ concentration

Question 4

What triggers the juxtaglomerular apparatus to produce renin?

Answer 4

Low tubular Na+ concentration

Low renal perfusion pressure

Question 5

What hormone is involved in decreasing sodium reabsorption?

Answer 5

Atrial Natriuretic Peptide (ANP)

Question 6

Where do you find a lot of ACE?

Answer 6

Lung Endothelium

Question 7

What effect does angiotensin II have on sodium reabsorption? Which parts of the nephron does it affect?

Answer 7

Increase sodium reabsorption in the PCT

Question 8

Describe the effects of aldosterone on absorption and secretion.

Answer 8

Increase Na+ reabsorption
Increases H+ secretion
Increases K+ secretion

Question 9

What is the result of aldosterone excess?

Answer 9

Hypokalemic Alkalosis

Question 10

How does aldosterone work? How does it cause an increase in sodium reabsorption?

Answer 10

Aldosterone is a steroid so it has a genomic effect and binds to type 1 intracellular receptors.
It relocalises the vesicles containing sodium transporters to the apical membrane
It also increases transcription and production of more sodium channels and Na+/K+ channels

Question 11

What are the consequences of hypoaldosteronism?

Answer 11

Reabsorption of sodium in the distal nephron is reduced
Increased urinary loss of sodium
ECF volume falls
Increased Angiotensin II and Vasopressin secretion
Low blood pressure, dizziness, palpitations, salt craving

Question 12

What are the consequences of hyperaldosteronism?

Answer 12

Increased sodium reabsorption in the distal nephron
Reduced urinary loss of sodium
ECF volume increases - HYPERTENSION
Reduced angiotensin and vasopressin secretion
Increased ANP and BNP

Question 13

What is Liddle’s Syndrome?

Answer 13

Mutation in the aldosterone dependent Na+ channel - the channel is permanently switched on resulting in sodium retention and HYPERTENSION

Question 14

What does low pressure stimulate?

Answer 14

RAS - more angiotensin II produced
Increase sympathetic activity
Increase ADH release

Question 15

How is ANP produced and what does it do?

Answer 15

ANP is produced by atrial stretch
It causes vasodilation of renal blood vessels
Inhibition of sodium absorption in the PCT and in collecting ducts
Inhibits release of renin and aldosterone

Question 16

How can GFR be affected to help lose sodium?

Answer 16

Increase GFR = more sodium removed

Question 17

Describe the effects of ACE inhibitors on sodium reabsorption.

Answer 17

ACE inhibitors reduce the amount of sodium reabsorption in the PCT (caused by Angiotensin II)
And they reduce the amount of sodium reabsorption in the DCT and collecting duct (due to indirect inhibition of aldosterone production)

Question 18

State five types of diuretics and where they act in the nephron.

Answer 18

Osmotic diuretics (glucose in diabetes and mannitol)
Carbonic Anhydrase Inhibitors
Loop Diuretics 
Thiazide Diuretics
Potassium Sparing Diuretics

Question 19

What is the basis behind diuretics with regards to tubular osmolarity?

Answer 19

They increase the tubular osmolarity so there is less of a gradient between the collecting duct and the interstitial compartment so less water is reabsorbed.

Question 20

What do loop diuretics do? Name a loop diuretic.

Answer 20

Furosemide - they block the Na+/K+/Cl- triple transporter

Question 21

What do thiazide diuretics do?

Answer 21

Inhibit Na+/Cl- cotransporter

Question 22

What do K+ sparing diuretics do? Name two.

Answer 22

Amiloride - Na+ channel blocker - prevents entry of Na+ from the tubule lumen
Spironolactone - aldosterone antagonist

Question 23

Why do you get a smaller natriuresis with K+ sparing diuretics?

Answer 23

Because they act on the collecting duct, which is only responsible for 2% of the reabsorption of Na+

Question 24

Why are they called K+ sparing diuretics?

Answer 24

They don’t cause increased excretion of K+

Question 25

What is a serious consequence of high extracellular K+?

Answer 25

It can cause depolarisation of membranes (e.g. resulting in arrhythmia)

Question 26

What stimulates the uptake of K+ into tissues?

Answer 26

INSULIN

Aldosterone and Adrenaline

Question 27

What stimulates K+ secretion?

Answer 27

Increase in plasma K+ concentration
Aldosterone (increase in)
Increase in tubular flow rate
Increase in pH

Question 28

How does tubular flow affect K+

Answer 28

secretion?
Principal cells have cilia that move with the flow. The movement of the cilium stimulates a protein called PDK1, which stimulates an increase in intracellular Ca2+ concentration
This stimulates the activity of the K+ channels
Flow is increased by diuretics, which is one of the problems with non-potassium sparing diuretics because they cause an increase in K+ secretion

Question 29

State some causes of hypokalaemia.

Answer 29

Diuretics
Diarrhoea
Surreptitious Vomiting
Genetics e.g. Gitelman’s syndrome

Question 30

State some causes of hyperkalaemia.

Answer 30

Ageing
Potassium-sparing diuretics
ACE inhibitors