Quamme G A, Carney S L, Wong N L, Dirks J H
Pflugers Arch. 1980 Jul;386(1):59-65. doi: 10.1007/BF00584188.
Tubular magnesium reabsorption was investigated by recollection micropuncture and in vivo microperfusion techniques in acutely thyroparathyroidectomized rats made magnesium deficient by dietary deprivation. Henle's loop which normally reclaims the major portion of filtered magnesium was examined by elevation of intraluminal magnesium concentration. The transport capacity in these conditions was significantly lower in magnesium deficient rats (41%) compared to normal animals (71%) at comparable magnesium delivery rates. Acute infusion of MgCl2 further depressed loop magnesium reabsorption independent of intraluminal magnesium delivery. Parathyroid hormone did not alter magnesium transport capacity in magnesium deficient rats but resulted in enhanced transport in acutely hypermagnesemic deficient rats. Calcium reabsorption followed a similar qualitative pattern as magnesium with respect to loop function and urinary excretion. These results are consistent with a depressed transport capacity for magnesium in the loop of Henle of magnesium deficient rats which is independent of intraluminal magnesium delivery and circulating parathyroid hormone level.
通过回收微穿刺和体内微灌注技术，对急性甲状旁腺切除且因饮食剥夺而缺镁的大鼠的肾小管镁重吸收进行了研究。通过提高管腔内镁浓度，对通常重吸收大部分滤过镁的亨利氏袢进行了检查。在可比的镁输送速率下，缺镁大鼠在这些条件下的转运能力（41%）明显低于正常动物（71%）。急性输注MgCl₂进一步降低了袢对镁的重吸收，且与管腔内镁输送无关。甲状旁腺激素并未改变缺镁大鼠的镁转运能力，但导致急性高镁血症缺镁大鼠的转运增强。就袢功能和尿排泄而言，钙重吸收与镁遵循相似的定性模式。这些结果与缺镁大鼠亨利氏袢中镁转运能力降低一致，这与管腔内镁输送和循环甲状旁腺激素水平无关。
