Regulation of Extrarenal Potassium Homeostasis by Insulin and Catecholamines

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.