Carney S L, Wong N L, Quamme G A, Dirks J H
J Clin Invest. 1980 Jan;65(1):180-8. doi: 10.1172/JCI109649.
Recollection of micropuncture experiments were performed on acutely thyroparathyroidectomized rats rendered magnesium deficient by dietary deprivation. Urinary magnesium excretion fell from a control of 15 to 3% of the filtered load after magnesium restriction. The loop of Henle, presumably the thick ascending limb, was the major modulator for renal magnesium homeostasis. The transport capacity for magnesium, however, was less in deficient rats than control animals. Absolute magnesium reabsorption increased with acute infusions of magnesium chloride but was always less in magnesium-deficient rats than control rats for any given filtered load, which suggests either a defect of a resetting of the reabsorption mechanism. Recollection micropuncture demonstrated that this was a characteristic of the loop of Henle. Proximal magnesium reabsorption remained unchanged at 15% of the filtered load and was unaffected by magnesium deficiency or acute magnesium repletion. Distal tubular magnesium reabsorption was limited during depletion and increased to a similar extent in control and deficient rats with enhanced magnesium delivery. Calcium reabsorption was not altered in magnesium deficiency; however, elevations of extracellular magnesium resulted in a specific inhibition of calcium reabsorption within the loop of Henle. These data suggest that overall control of renal magnesium reabsorption occurs within the loop of Henle and that the proximal tubule reabsorbs a constant fraction of the filtered load despite variations in body magnesium status.
对通过饮食剥夺造成镁缺乏的急性甲状旁腺切除大鼠进行了微穿刺实验回顾。镁限制后，尿镁排泄从对照时滤过负荷的15%降至3%。亨利袢，可能是厚壁升支，是肾镁稳态的主要调节部位。然而，缺镁大鼠的镁转运能力低于对照动物。急性输注氯化镁时，绝对镁重吸收增加，但在任何给定的滤过负荷下，缺镁大鼠的绝对镁重吸收总是低于对照大鼠，这表明重吸收机制的重置存在缺陷。微穿刺实验回顾表明，这是亨利袢的一个特征。近端镁重吸收保持在滤过负荷的15%不变，不受镁缺乏或急性镁补充的影响。远端肾小管镁重吸收在缺镁期间受限，在镁输送增加的对照大鼠和缺镁大鼠中增加程度相似。镁缺乏时钙重吸收未改变；然而，细胞外镁升高导致亨利袢内钙重吸收受到特异性抑制作用。这些数据表明，肾镁重吸收的总体控制发生在亨利袢内，并且尽管机体镁状态存在变化，近端小管仍重吸收滤过负荷的恒定比例。
