Role of the loop segment in the urinary concentrating defect of hypercalcemia.
Role of the loop segment in the urinary concentrating defect of hypercalcemia.
复制标题
环段在高钙血症尿浓缩缺陷中的作用。
DOI：
10.1038/ki.1986.96
复制
发表时间：
1986
影响因子：
19.6
通讯作者：
Luke,RG
中科院分区：
文献类型：
--
作者：
Galla,JH;Booker,BB;Luke,RG
袢段在高钙血症尿浓缩缺陷中的作用。高钙血症与尿浓缩能力受损有关。为了探讨高钙血症损害Henle袢中氯离子转运的机制，我们对Sprague-Dawley大鼠进行了在体微灌注，通过葡萄糖酸钙输注使其急性高钙血症（12.1 ± 0.1 mg/dl）。对照组大鼠输注葡萄糖酸钠，血浆钙水平正常（8.0 ± 0.2 mg/dl）。与对照组相比，高钙血症患者的氯化物重吸收分数降低（61 ± 4至50 ± 3%; P < 0.05），早期远端氯化物增加（74 ± 6至98 ± 3 mEq/L）（P < 0.001）。在高钙血症时，注射维拉帕米不能增加氯离子重吸收分数（49 ± 4%; P < 0.05）或降低早期远端氯离子（95 ± 2; P < 0.05）至对照值。同样，吲哚美辛也没有改善氯离子重吸收分数（48 ± 4%; P < 0.05）或远端氯离子浓度（93 ± 7; P < 0.05）。在输注Ringers HCO 3的对照大鼠中，向灌注液中添加8.0 mEq/L钙可增加早期远端钙（0.22至3.11 mEq/L），但与氯化物重吸收分数（-6 ± 6%）无变化和早期远端氯化物轻微降低（-9 ± 3 mEq/L; P < 0.05）相关。这些数据是一致的假设，即升高的血浆，而不是管腔钙，浓度损害氯离子重吸收的环段，主要是ADH刺激的组件。这可能在高钙血症的尿浓缩缺陷中起重要作用。
Role of the loop segment in the urinary concentrating defect of hypercalcemia. Hypercalcemia is associated with impaired urinary concentrating ability. To explore the mechanism(s) by which hypercalcemia impairs chloride transport in the loop of Henle, we carried out in vivo microperfusion of the loop segment in Sprague–Dawley rats rendered acutely hypercalcemie (12.1 ± 0.1 mg/dliter) by calcium gluconate infusion. Control rats were infused with sodium gluconate and had normal plasma calcium (8.0 ± 0.2 mg/dliter). Compared to control, fractional chloride reabsorption was decreased (61 ± 4 to 50 ± 3%; P < 0.05) and early distal chloride increased 74 ± 6 to 98 ± 3 mEq/liter (P < 0.001) in hypercalcemia. During hypercalcemia, infusion of verapamil failed to increase fractional chloride reabsorption (49 ± 4%; P < 0.05) or decrease early distal chloride (95 ± 2; P < 0.05) toward control values. Similarly, indomethacin did not improve fractional chloride reabsorption (48 ± 4%; P < 0.05) or distal chloride concentration (93 ± 7; P < 0.05). In control rats infused with Ringers HCO3, the addition of calcium 8.0 mEq/liter to the perfusate increased early distal calcium (0.22 to 3.11 mEq/liter) but was associated with no change in fractional chloride reabsorption (-6 ± 6%) and a slight decrease in early distal chloride (-9 ± 3 mEq/liter; P < 0.05). These data are consistent with the hypothesis that an elevated plasma, not luminal calcium, concentration impairs chloride reabsorption in the loop segment, primarily the ADH–stimulated component. This may have an important role in the urinary concentrating defect of hypercalcemia.