Title: Hormonal and pharmacological modification of plasma potassium homeostasis
Abstract: Abstract Human skeletal muscles contain the largest single pool of K + in the body (2600 mmol, 46 times the total K + content of the extracellular space). Intense exercise may double arterial plasma K + in one min. This is because of excitation‐induced release of K + from the working muscle cells via K + channels. This hyperkalemia is rapidly corrected by reaccumulation of K + into the muscle cells via Na + ,K + pumps, often leading to hypokalemia. Hyperkalemia may also arise from muscle cell damage, excessive oral or intravenous administration of K + , acidosis, renal failure, depolarization of muscle cells with succinyl choline, activation of K + channels by fluoride poisoning, hyperkalemic periodic paralysis, malignant hyperthermia, inhibition of the Na + ,K + pumps by digitalis glycosides or treatment with nonselective beta blockers. Hyperkalemia may cause arrhythmia and can be treated with beta 2 agonists, insulin or hemodialysis. Hypokalemia may be induced by the stimulation of the Na + ,K + pumps in skeletal muscles seen postexercise, or by catecholamines, beta 2 agonists, pheochromocytoma, theophylline, caffeine or insulin, by sepsis, myocardial infarction, trauma, burns and heart failure. Rare causes are hypokalemic periodic paralysis, inhibition of K + channels by barium, chloroquine or barbiturates. Hypokalemia often reflects dietary K + deficiency, alkalosis, renal or gastrointestinal loss of K + . Hypokalemia is more likely to cause arrhythmia than hyperkalemia and can be treated by oral or intravenous administration of K + under frequent control of electrocardiogram and plasma K + . Because of their size and high contents of K + , Na + ,K + pumps and K + channels, the skeletal muscles play a central role in the acute, from min‐to‐min ongoing regulation of plasma K + . This is decisive for the maintenance of muscle contractility and heart function.