Knepper M A
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603, USA.
Am J Physiol. 1998 Sep;275(3):F332-3. doi: 10.1152/ajprenal.1998.275.3.F332.
Urinary concentrating capacity is regulated in part by a long-term adaptational process involving changes in the absolute abundance of the aquaporin-2 water channel in collecting duct cells. Alterations in aquaporin-2 abundance play key roles in the pathophysiology of several water balance disorders. Escape from the antidiuretic action of vasopressin, e.g. in the syndrome of inappropriate antidiuretic hormone secretion, involves a selective downregulation of aquaporin-2 expression. Excessive water retention causing hyponatremia in volume-expanded states such as congestive heart failure appears to be due in part to a failure of this escape mechanism.
尿浓缩能力部分受一个长期适应性过程的调节，该过程涉及集合管细胞中水通道蛋白-2水通道绝对丰度的变化。水通道蛋白-2丰度的改变在几种水平衡紊乱的病理生理学中起关键作用。对血管加压素抗利尿作用的逃逸，例如在抗利尿激素分泌不当综合征中，涉及水通道蛋白-2表达的选择性下调。在充血性心力衰竭等容量扩张状态下导致低钠血症的水潴留过多，似乎部分是由于这种逃逸机制的失效。
