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Flashcards in Sodium and Potassium Balance Deck (30)
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State the relative amounts of sodium reabsorbed in different parts of the nephron.

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


Describe the relationship between GFR and sodium reabsorption.

The greater the GFR the greater the sodium reabsorption


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

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


What triggers the juxtaglomerular apparatus to produce renin?

Low tubular Na+ concentration
Low renal perfusion pressure


What hormone is involved in decreasing sodium reabsorption?

Atrial Natriuretic Peptide (ANP)


Where do you find a lot of ACE?

Lung Endothelium


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

Increase sodium reabsorption in the PCT


Describe the effects of aldosterone on absorption and secretion.

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


What is the result of aldosterone excess?

Hypokalemic Alkalosis


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

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


What are the consequences of hypoaldosteronism?

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


What are the consequences of hyperaldosteronism?

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


What is Liddle's Syndrome?

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


What does low pressure stimulate?

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


How is ANP produced and what does it do?

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


How can GFR be affected to help lose sodium?

Increase GFR = more sodium removed


Describe the effects of ACE inhibitors on sodium reabsorption.

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)


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

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


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

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.


What do loop diuretics do? Name a loop diuretic.

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


What do thiazide diuretics do?

Inhibit Na+/Cl- cotransporter


What do K+ sparing diuretics do? Name two.

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


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

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


Why are they called K+ sparing diuretics?

They don't cause increased excretion of K+


What is a serious consequence of high extracellular K+?

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


What stimulates the uptake of K+ into tissues?

Aldosterone and Adrenaline


What stimulates K+ secretion?

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


How does tubular flow affect K+

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


State some causes of hypokalaemia.

Surreptitious Vomiting


State some causes of hyperkalaemia.

Potassium-sparing diuretics
ACE inhibitors