Seminars in Nephrology
Volume 28, Issue 3 , Pages 289-296, May 2008

Vasopressin and Aquaporin 2 in Clinical Disorders of Water Homeostasis

  • Robert W. Schrier, MD

      Affiliations

    • Corresponding Author InformationAddress reprint requests to Robert W. Schrier, Division of Renal Diseases and Hypertension—School of Medicine, Department of Medicine, University of Colorado at Denver Health Sciences Center, 4200 E Ninth Ave, Box B173, Denver, CO 80262-3706.

Division of Renal Diseases and Hypertension—School of Medicine, Department of Medicine, University of Colorado at Denver Health Sciences Center, Denver, CO

Summary 

Impaired urinary dilution leading to water retention and hyponatremia may occur in patients with cardiac failure, cirrhosis, pregnancy, oxytocin administration, hypothyroidism, glucocorticoid, and mineralocorticoid deficiency. The mechanisms for these defects predominantly involve the nonosmotic stimulation of arginine vasopressin release with up-regulation of aquaporin 2 water channel expression and trafficking to the apical membrane of the principal cells of the collecting duct. These perturbations are reversed by V2 vasopressin receptor antagonists. In contrast, urinary concentration defects leading to polyuria are vasopressin resistant. They may involve several factors, such as impaired countercurrent concentration secondary to down-regulation of Na-K-2Cl cotransporter. Vasopressin-resistant down-regulation of aquaporin 2 expression has also been described as a factor in impaired urinary concentration.

Keywords: Water channels, antidiuretic hormone, polyuria, hyponatremia

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PII: S0270-9295(08)00052-1

doi:10.1016/j.semnephrol.2008.03.009

Seminars in Nephrology
Volume 28, Issue 3 , Pages 289-296, May 2008