Regulation of 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

what is the most important solute.

Answer 3

Sodium most prevalent, and important, solute in the ECF.

Question 4

What are the effects of

changing sodium levels

Answer 4

Increased dietary sodium
Increased osmolarity 
(but the body can’t let this happen)
Increased ECF volume  
Increased blood volume and pressure 

Decreased dietary sodium
Decreased osmolarity 
(but the body can’t let this happen)
Decreased ECF volume  
Decreased blood volume and pressure

Question 5

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

Answer 5

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 6

What triggers the juxtaglomerular apparatus to produce renin?

Answer 6

Low tubular Na+ concentration

Low renal perfusion pressure

Question 7

What hormone is involved in decreasing sodium reabsorption?

Answer 7

Atrial Natriuretic Peptide (ANP)

Question 8

Where do you find a lot of ACE?

Answer 8

Lung Endothelium

Question 9

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

Answer 9

Increase sodium reabsorption in the PCT

Question 10

Describe the effects of aldosterone on absorption and secretion.

Answer 10

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

Question 11

What is the result of aldosterone excess?

Answer 11

Hypokalemic Alkalosis

Question 12

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

Answer 12

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 13

What are the consequences of hypoaldosteronism?

Answer 13

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

Question 14

What are the consequences of hyperaldosteronism?

Answer 14

Increased sodium reabsorption in the distal nephron
Reduced urinary loss of sodium
ECF volume increases - HYPERTENSION
Reduced angiotensin and vasopressin secretion , renin
Increased ANP and BNP
Leads to high blood pressure, muscle weakness, polyuria and thirst

Question 15

What is Liddle’s Syndrome?

Answer 15

Inherited disease of high blood [ressure
Mutation in the aldosterone dependent Na+ channel - the channel is permanently switched on resulting in sodium retention and HYPERTENSION

Question 16

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

Answer 16

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
Synthesised and released from the adrenal cortex
Released in response to Angiotensin ll,
decrease in blood pressure (via baroreceptors)
decreased osmolarity of ultrafiltrate

Question 17

How can GFR be affected to help lose sodium?

Answer 17

Increase GFR = more sodium removed

Question 18

what are the drugs that can affect the tubular system where they act in the nephron.

Answer 18

ACE inhibitors: lower blood pressure . Doesn’t only affect kidneys but also other places around the body.

Diuretics:
Osmotic diuretics (glucose in diabetes and mannitol): increase osmolarity in the tubular system and so allow less water and sodium to exit via the para-cellular routes.
Carbonic Anhydrase Inhibitors : prevent the production of protons and block pumps in the PCT
Loop Diuretics : usually block triple transporter in the ascending loop
Thiazide Diuretics: DCT
Potassium Sparing Diuretics: block K+/Cl- co-transporters which leads to a change in calcium uptake because less sodium is taken in.

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

How does tubular flow affect K+secretion?

Answer 27

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 28

State some causes of hypokalaemia.

Answer 28

Diuretics
Diarrhoea
Surreptitious Vomiting
Genetics (Gitelman’s syndrome; mutation in the Na/Cl transporter in the distal nephron)

Question 29

State some causes of hyperkalaemia.

Answer 29

Ageing
Potassium-sparing diuretics
ACE inhibitors

Question 30

what is the immediate response to dietary potassium

Answer 30

is for it to be pumped into cells via Na+K+ATPase, over time it equilibrates and the output at the collecting duct ranges between 1%-80% of what goes into the tubular system.

Question 31

what is the variation stimulated by?

Answer 31

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

Question 32

what are the mechanisms by which potassium secretion is regulated?

Answer 32

-secreted by principal cells

1. Na+K+ATPase activity
2. Permeability of potassium channel (aldosterone)
3. tubular flow (flow sensors primary cilium are linked to potassium

Question 33

what do bararecptors measure and where?

Answer 33

Measure on the low pressure and high pressure sides, measure stretch of vessels/

Low pressure: atria, right ventricle, pulmonary vasculature
High pressure: carotid sinus, aortic arch and JGA