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Treatment with thiazides and loop diuretics increase the urinary excretion of potassium and magnesium and the body content of these ions are reduced after long-term treatment. The diuretic-induced magnesium deficiency influences the potassium metabolism. Magnesium is a necessary activator of Na-K-ATPase, which supplies the Na-K pump with energy. Lack of magnesium will therefore impair the pumping of sodium out of the cell and of potassium into the cell. The change of the relationship between extra and intracellular potassium may induce cardiac arrhythmias. Certain groups of patients, such as patients on digitalis therapy, patients with secondary hyperaldosteronism, elderly patients with insufficient dietary habits, and heavy drinkers, run an additional risk of developing potassium/magnesium disturbances. In young patients with uncomplicated essential hypertension, the risk is probably very small.