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Am J Physiol Renal Physiol 275: F332-F333, 1998;
0363-6127/98 $5.00
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Vol. 275, Issue 3, F332-F333, September 1998

BRIEF REVIEW
Long-term regulation of urinary concentrating capacity1

Mark A. Knepper

Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603

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.

cortical collecting duct; vasopressin; water permeability

1 This report is the fourth in a series of minireviews, which are based on a symposium on the urinary concentrating mechanism, held at Experimental Biology '97 in New Orleans, LA.




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