Control Of Potassium Flashcards
Where is most potassium?
Inside cells (98% of K) -mostly in skeletal muscles
[K+] = 120-150mmol/L
ECF = only 2% (3-5mmol/L)
This means that a shift of 1% of ICF K+ to ECF would raise ECF [K+] by 50%.
How is the difference between ECF and ICF maintained?
NaKATPase - maintaining it is critical
Why is maintaining ECF [K+] so critical?
Because of its effect on the resting membrane potential.
Hence its effect on excitability of cardiac tissue.
Hence the risk of life threatening arrhythmias with hyperkalaemia and hypokalaemia
How is ECF K+ regulated?
Immediate control - by internal balance - moves K+ between ECF and ICF
Longer term, overall K+ balance - by external balance (match input with output) adjusting renal secretions.
List some foods that are rich in potassium
Raisins Honey dew melon Banana Orange Tomato Potato chips Baked potato Milk
How does your body control potassium following a meal?
The intestines and colon absorb dietary K+ - This means ECF K+ will increase a little bit.
BUT, 4/5th moves into cells within minutes to stop [K+] increasing my too much.
After a slight delay kidneys begin to excrete K+ -excretion is complete in 6-12 hours.
New research also suggest that the gut has some influence in controlling after meal K+ secretion
How does potassium enter and leave cells?
Internal balance is the net result of the movement of K+ into and out of cells.
K+ moves from ECF into cells via NaKATPase
K+ moves out of cells into ECF via K+ channels (channels which determine the K+ permeability of the cell membrane)
What factors increase the K+ uptake by cells?
Hormones
- Insulin (rises anyway with a meal)
- Aldosterone (secreted from suprarenal gland -stimulated by RAAS)
- Catecholamines (B2 agonist)
Increased [K+] in ECF
Alkalosis pH - low ECF [H+] - K+ shift into cells.
What factors provost the K+ shift out of cells?
Exercise
Cel lysis
Increase in ECF osmolality (e.g. diabetes)
Low ECF [K+]
Acidosis - increase in ECF [H+] camisoles a K+ shift and movement out of the cells.
How does insulin cause an increase in K+ uptake?
K+ in splanchnic blood stimulates insulin secretion by pancreas
Insulin increases Na-K-ATPase activity - increases K+ uptake by muscle cells and liver.
I.V insulin + Dextrose is used to treat hyperkalaemia
How does aldosterone cause an increase in K+ uptake?
K+ in blood stimulates aldosterone secretion which stimulates the uptake of K+ via NaKATPase.
How do catecholamines stimulate the uptake of K+?
Act via B2 adrenoreceptors which stimulate Na-K-ATPase and cellular uptake of K+
What happens to the K+ concentration in exercise?
Net release of K+ during recovery phase of action potential, K+ exits the cell.
Also skeletal muscle damage during exercise releases K+.
This means that the increase plasma [K+] is proportional to the intensity of the exercise.
Uptake by non-contracting tissues prevents dangerously high hyperkalaemia.
Exercise and trauma also increases catecholamines, high offset ECF [K+] rise by increasing K+ uptake by other cells.
Cessation of exercise results in a rapid decrease in plasma [K+], often to under 3mmol/L.
How does acidosis lead to hyperkalaemia?
In acidosis, H+ shift into cells and there is a reciprocal shift of K+ out of the cells.
The opposite can occur and hyperkalaemia can cause acidosis.
How does alkalosis lead to hypokalaemia?
Alkalosis causes a shift of H+ out of the cells.
This means there is a reciprocal shift of K+ Ito the cells.
The opposite can occur and hypokalaemia can cause alkalosis.
Where abouts in the nephron is potassium mainly regulated?
Late distal tubule an cortical collecting duct
How does the kidney handle potassium?
Most of the K+ is reabsorbed.
- 67% in PCT
- 20% in Thick ascending limb of LoH
- Rest in DT and collecting duct
Some K+ is secreted into the distal tubule and cortical collecting duct - this can be varied and controlled so it is this K that will appear in the urine and not that which is reabsorbed.
How will K+ reabsorbtion / secretion change if you have a low K+ diet?
The reabsorbtion mainly stays the same.
The secretion in the principle cells of DCT and cortical collecting duct will be minimised.
How is K+ secreted in the distal tubule and collecting duct?
It is secreted by principle cells.
NaKATPase activity in the basolateral membrane increase [K+] and decrease [Na+].
High intracellular K+ creates a chemical gradient for secretion.
Na+ moves from lumen into cell down its concentration gradient (via apical ENaC) creating an electrical gradient.
Together create a favourable electrochemical gradient for K+ secretion via apical K+ channels.
What tubular factors affect K+ secretion by principle cells?
ECF [K+]
- Directly stimulates NaKATPase and increases permeability of apical K+ channels.
- Also stimulates aldosterone secretion
Aldosterone -Increases: transcription of relevant proteins K+ channels ENaC in apical membrane
Acid base status
-Acidosis - decreases K+ secretion, inhibits NaKATPase and decrease K+ channel permeability. Alkalosis does the opposite.
What luminal factors affect K+ secretion by principle cells?
Increased distal tubular flow rate - washes away luminal K+ and increases K+ loss.
Increases Na delivery to distal tubule - more Na absorbed which results in more Na absorbed and therefore more K+ loss. (E.g. diuretic - ferosimide bocks Na absorption in thcika spending limb so more available downstream)
What cells absorb K+ in the DT and CD?
Intercalated cells.
This is an active process that is mediated by the HKATPase in the apical membrane.
What are some of the effects of changes in ECF [K+]?
Alter cell membrane resting potential
Alter neuro muscular excitability
- Problems with cardiac conduction and pacemaker automaticity
- Alter neuronal function
- Alter skeletal muscle function
- Alter smooth muscle function
Results in arrhythmias, cardiac arrest, muscle paralysis.
BUT, usually pick it up quite late so need to know situations that this is likely to occur.
What could cause hyperkalaemia?
Increased intake (unlikely) - only if renal dysfunction is also present. Unless inappropriate dose of IV K+
Decreased renal excretion (more likely)
- Acute of chronic kidney injury
- Drugs that block K+ excretion (most frequent) - ACE inhibitors, K+ sparing diuretics
- Low aldosterone state (addison’s disease).
Also internal shift.
