Takagi J, Otake K, Nakao N, Takashashi M, Hirooka Y
Department of Laboratory Medicine, Aichi Medical University, Aichi, Japan.
Horm Metab Res. 2003 Jan;35(1):62-6. doi: 10.1055/s-2003-38393.
Aquaporin-2, a water-channel protein, is known to increase water permeability due to vasopressin binding to V2 receptors at the renal collecting duct and is excreted into the urine. It is still unclear whether a hyponatremic state is caused by vasopressin-dependent aquaporin-2 in patients clinically diagnosed with the syndrome of inappropriate secretion of antidiuretic hormone. To determine this, we measured urinary aquaporin-2 and vasopressin by radioimmunoassay in normonatremic or hyponatremic patients after cerebral infarction and in healthy controls. In the normonatremia group, urinary aquaporin-2 and plasma AVP levels were higher than in controls. In the hyponatremia group, plasma AVP was relatively high despite low plasma osmolality in each patient. However, urinary aquaporin-2 in hyponatremia was significantly increased when compared with the other two groups. In conclusion, AQP-2 increment does not directly reflect non-osmotic AVP secretion in a hyponatremic state. This result indicates that the urinary excretion of AQP-2 is not only AVP-dependent in hyponatremic states.
水通道蛋白2是一种水通道蛋白，已知其可因血管加压素与肾集合管的V2受体结合而增加水通透性，并被排泄到尿液中。对于临床诊断为抗利尿激素分泌不当综合征的患者，低钠血症状态是否由血管加压素依赖性水通道蛋白2引起仍不清楚。为了确定这一点，我们通过放射免疫分析法测量了脑梗死患者正常血钠或低血钠状态下以及健康对照者的尿水通道蛋白2和血管加压素。在正常血钠组中，尿水通道蛋白2和血浆抗利尿激素水平高于对照组。在低血钠组中，尽管每位患者血浆渗透压较低，但血浆抗利尿激素相对较高。然而，与其他两组相比，低血钠组的尿水通道蛋白2显著增加。总之，在低钠血症状态下，水通道蛋白2的增加并不直接反映非渗透性抗利尿激素的分泌。这一结果表明，在低钠血症状态下，水通道蛋白2的尿排泄不仅依赖于抗利尿激素。
