Wester P O, Dyckner T
Acta Pharmacol Toxicol (Copenh). 1984;54 Suppl 1:59-65. doi: 10.1111/j.1600-0773.1984.tb03634.x.
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.
噻嗪类利尿剂和袢利尿剂治疗会增加钾和镁的尿排泄量,长期治疗后这些离子的体内含量会降低。利尿剂引起的镁缺乏会影响钾代谢。镁是钠钾ATP酶的必要激活剂,为钠钾泵提供能量。因此,镁缺乏会损害钠从细胞内泵出以及钾进入细胞的过程。细胞内外钾关系的改变可能诱发心律失常。某些患者群体,如接受洋地黄治疗的患者、继发性醛固酮增多症患者、饮食习惯不良的老年患者以及酗酒者,发生钾/镁紊乱的额外风险更高。在无并发症的原发性高血压年轻患者中,这种风险可能非常小。