Vezzoli G, Reina M C, Zerbi S, Spaventa R, Soldati L, Cusi D, Bianchi G
Department of Nephrology Dialysis and Hypertension, S. Raffaele Scientific Institute, University of Milano, Italy.
Biochem Biophys Res Commun. 1995 Dec 26;217(3):1099-104. doi: 10.1006/bbrc.1995.2882.
Increased erythrocyte (Ca+Mg)ATPase activity was previously observed in idiopathic hypercalciuria. In order to verify if this alteration is a primary or a secondary event, we studied Sr influx in erythrocytes from subjects with idiopathic hypercalciuria. (Ca+Mg)ATPase activity was significantly higher in hypercalciuric than in hypercalciuric than in normocalciuric subjects whereas no difference in Sr influx was found between the two groups. (Ca+Mg)ATPase activity positively correlated with the erythrocyte Sr content found after 5 min of incubation and with urine Ca excretion. The normal Sr permeability suggests that (Ca+Mg)ATPase is primarily altered in idiopathic hypercalciuria. The primary increase of (Ca+Mg)ATPase activity may enhance passive Ca influx by reduction of cellular Ca concentration. It may induce a defect in cellular Ca metabolism that may cause idiopathic hypercalciuria by stimulating bone Ca turn-over and enteral Ca absorption.
先前在特发性高钙尿症患者中观察到红细胞(钙+镁)ATP酶活性增加。为了验证这种改变是原发性还是继发性事件,我们研究了特发性高钙尿症患者红细胞中的锶流入情况。高钙尿症患者的(钙+镁)ATP酶活性显著高于正常钙尿症患者,而两组之间的锶流入没有差异。(钙+镁)ATP酶活性与孵育5分钟后发现的红细胞锶含量以及尿钙排泄呈正相关。正常的锶通透性表明(钙+镁)ATP酶在特发性高钙尿症中主要发生改变。(钙+镁)ATP酶活性的原发性增加可能通过降低细胞内钙浓度来增强被动钙流入。它可能导致细胞钙代谢缺陷,通过刺激骨钙周转和肠道钙吸收而引起特发性高钙尿症。