Figure

Extrarenal potassium homeostasis: insulin and catecholamines. Schematic representation of the cellular mechanisms by which insulin and ^-adrenergic stimulation promote potassium uptake by extrarenal tissues. Insulin binding to its receptor results in hyperpo-larization of cell membranes (1), which facilitates potassium uptake. After binding to its receptor, insulin also activates Na+-K+-ATPase pumps, resulting in cellular uptake of potassium (2). The second messenger that mediates this effect has not yet been identified. Catecholamines stimulate cellular potassium uptake via the | adrenergic receptor (I2R). The generation of cyclic adenosine monophosphate (3', 5' cAMP) activates Na+-K+-ATPase pumps (3), causing an influx of potassium in exchange for sodium [10]. By inhibiting the degradation of cyclic AMP, theophylline potentiates catecholamine-stimulated potassium uptake, resulting in hypokalemia (4).

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