Regulation of potassium balance

What foods are high in potassium?

pinto beans

tomato paste

raisins

baked potato

steak

Internal vs external potassium balance

Internal: (quick process) Controls distribution of potassium between ECF and ICF

External (slow process): Regulates renal potassium excretion to balance potassium intake

Factors that shift potassium into cells

Factors that shift potassium outside of cells

How does insulin cause potassium to move into cells

increased plasma [K+] depolarises β pancreatic cells→ release insulin → stimulates K+ uptake by muscle cells and liver via an increase in Na- K-ATPase

How does acidosis and alkalosis affect potassium levels?

Acidosis: shift of H + into cells → reciprocal K+ shift out of cells → Hyperkalaemia

low pH blocks Na+ - H+and Na/HCO3- → more H+ in cell → inhibits Na+/K+ pump and Na-K-Cl transporter

Alkalosis: shift of H + out of cells → reciprocal K+ shift in to cells → Hypokalaemia

How does a high plasma osmolarity affect potassium?

1. Water moves from cells into ECF (because of the osmotic gradient)
2. Cell shrinks
3. Increased [K+ ] in ICF
4. K+ leaves down concentration gradient

What other factors can cause hyperkalaemia?

cell lysis

strenuous exercise: K+ is released from skeletal muscle into ECF

In what ways do we regulate external potassium balance?

-ve feedback regulation: Reactive dependent from k+ conc 

food-forward regulation: reactive independent from K+ conc 

Predicative: follows circadian rhythm so kaliuresis is higher in the day

Where is potassium usuaully reabsorbed and secreted in the nephron?

reabsorbed: mostly PCT + loop of Henle

secreted: distal tubule + cortical collecting duct (unless K+ is low then it can reabsorb)

How is potassium secreted in the principal cells of the collecting duct?

Na + is reabsorbed through ENaC

Stimulates basolateral Na + /K+ - ATPase → K+ actively pumped into the cell
from the peritubular fluid

K+ (passively) secreted at the apical membrane by K+ /Cl - cotransporters and K+ channels (ROMK)

What peritubular factors affect principal cell potassium secretion?

High Plasma [K+ ]:

•  Directly stimulates Na-K-ATPase

• ↑permeability of apical K+ channels

• stimulates aldosterone secretion

Aldosterone:

• ↑ Na-K-ATPase

• ↑ ENaC in apical membrane

•  ↑ K+ channels

Acid base balance

• Acidosis:↓ K+ secretion: inhibits Na-K-ATPase, ↓ K+ channel
  permeability

• Alkalosis: ↑ K+ secretion: stimulates Na-K-ATPase, ↑ K+
  channel permeability+ channels

What luminar factors affect principal cell potassium secretion?

Flow of distal tubular fluid: 

• Increased flow rate increases K+ secretion

• Decreased flow rate reduces K+ secretion

[Na+ ] delivery to distal tubule:

• Increased [Na + ] delivery to distal tubule → increases K+ secretion

• Decreased [Na + ] delivery to distal tubule → decreases K+ secretion

How does potassium get absorbed in the intercalated cells?

** alpha- intercelated cells

K+ actively absorbed from the duct lumen through an apical H + -K+ -ATPase (** if a lot of K+ is reabsorbed there is an increase in H+ secretion → alkalosis)

K+ exit from intercalated cells into the blood is mediated by a K+ channel

Why would you get pseudohyperkalaemia?

artefactual increase in serum K+ caused by the release of K+ during venepuncture (haemolysis) 

What might lead to redistribution of potassium from ICF to ECF

Acidosis (inhibits Na +/H+ exchange)

Diabetic ketoacidosis (inhibits Na +/K+-ATPase; increases plasma osmolality)

Drugs: Beta blockers, digoxin (inhibit Na +/K+- ATPase)

What can cause impaired renal potassium excretion?

Acute or chronic renal failure

Tubular disease

Lack of aldosterone (Addison’s disease)

ACE inhibitors/ ARBs

How do you manage hyperkalaemia?

Causes of hypokalaemia?

Decreased intake: Alcoholism; anorexia

Increased loss:

• Extra-renal loss: GI – diarrhoea/vomiting

• Renal loss
  • Diuretic drugs
  • Osmotic diuresis
  • High aldosterone levels
  • Hypomagnesemia
  • Renal potassium transport defects

Symptoms of hypokalaemia

Heart: altered excitability → arrhythmias

Gastrointestinal: neuromuscular dysfunction →constipation, paralytic ileus

Skeletal muscle: neuromuscular dysfunction → muscle cramps, weakness

Renal: dysfunction of collecting duct cells → unresponsive to ADH →
nephrogenic diabetes insipidus

Treatment of hypokalaemia

1. identify underlying cause

2. potassium replacement: oral/ IV (if severe ,2.5mmol/l)