Regulation of Extrarenal Potassium Homeostasis by Insulin and Catecholamines

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6 Scopus citations


The chapter focuses on the hormonal control of extrarenal potassium (K) homeostasis, using insulin and catecholamines as model systems. Insulin is an important regulator of K uptake by extrarenal tissues, muscle and liver. In the absence of insulin or if there exists resistance to the action of insulin, extrarenal K homeostasis will be impaired. Insulin lack will be associated with a rise in the plasma glucose concentration. The resultant hypertonicity will cause the translocation of water and K out of cells into the extracellular compartment, leading to hyperkalemia. The insulin deficiency be particularly severe, ketoacidosis may ensue and the metabolic acidemia will exacerbate the hyperkalemia via two mechanisms: K will move out of cells in exchange for hydrogen (H), which has entered the cell to be buffered by intracellular proteins, and the increase in blood H ion concentration will directly inhibit K secretion by the distal tubule and collecting duct. In addition to insulin deficiency, diabetics commonly have a defect in aldosterone secretion. If present, this will lead to an impairment in K uptake by extrarenal tissues, as well as a decrease in renal K excretion. The sympathetic nervous system and circulating catecholamines have been shown to play the most important role in the maintenance of extrarenal K homeostasis. The cellular mechanisms via which catecholamines regulate extrarenal K uptake have been reviewed in the chapter.

Original languageEnglish (US)
Pages (from-to)299-329
Number of pages31
JournalCurrent Topics in Membranes and Transport
Issue numberC
StatePublished - Jan 1987
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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