Almost all of the body’s potassium stores are intracellular, with a high concentration of potassium maintained in the intracellular fluid by the Na+ -K+ -ATPase pump exchanging it for sodium. This is important in maintaining cellular membrane potential and small changes in the extracellular potassium level affect the normal function of cells, particularly of muscle cells, e.g. myocardium and skeletal muscle.
Various factors can act to change total body stores of potassium:
· Intake can be increased by a potassium-rich diet or by oral or intravenous supplements.
· Potassium is found in high levels in gastric juice and most of this is reabsorbed in the small intestine. A small amount of potassium is lost in the stool. Vomiting or diarrhoea can reduce total body potassium.
· The kidneys are the main route of excretion of potassium, excreting 90% of the intake. Potassium excretion by the kidneys is controlled by aldosterone, which acts on the distal tubules and collecting ducts to increase sodium reabsorption and potassium excretion. Disturbances of the renin–angiotensin–aldosterone system can therefore cause alterations in the potassium level. In severe renal failure, when 90% of the renal function is lost, the kidneys become unable to excrete sufficient potassium.
The normal intracellular to extracellular ratio of potassium is affected by acid–base status, insulin, catecholamines, aldosterone and drugs.
In most tissues, including the kidney, potassium and hydrogen ions compete with each other at the cell membrane to be exchanged for sodium. If the hydrogen concentration is high (acidotic conditions), the kidney excretes hydrogen ions in preference to potassium; in the tissues, hydrogen ions compete with potassium to be taken up by the cells, so extracellular potassium concentration rises (hyperkalaemia). As the acidosis is corrected, potassium is taken up by the cells and may cause hypokalaemia. Conversely, in metabolic alkalosis potassium is excreted in exchange for hydrogen ions, leading to hypokalaemia.
Insulin and activation of β2 receptors tend to drive potassium into cells, lowering the serum potassium concentration.