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Am J Physiol Renal Physiol 274: F1161-F1166, 1998;
0363-6127/98 $5.00
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Vol. 274, Issue 6, F1161-F1166, June 1998

Escape from vasopressin-induced antidiuresis: role of vasopressin resistance of the collecting duct

Carolyn A. Ecelbarger1, Chung-Lin Chou1, Alanna J. Lee1, Susan R. DiGiovanni2, Joseph G. Verbalis3, and Mark A. Knepper1

1 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1603; 2 Division of Nephrology, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia 23298; and 3 Division of Endocrinology, Georgetown University, Washington, District of Columbia 20007

Previously, we demonstrated that escape from vasopressin-induced antidiuresis ("vasopressin escape") in rats is associated with a large, selective decrease in whole kidney expression of aquaporin-2, the vasopressin-regulated water channel. Here, we show that isolated perfused inner medullary collecting ducts (IMCDs) from vasopressin-escape rats {desamino-[D-arginine]vasopressin (DDAVP)/water-loaded} have dramatically reduced vasopressin-dependent osmotic water permeabilities [46% of control rats (DDAVP alone)], which coincides with a fall in inner medullary aquaporin-2 protein abundance as measured by immunoblotting in the opposite kidney. Furthermore, we demonstrate in IMCD suspensions that cAMP accumulation in response to DDAVP is substantially reduced in the vasopressin-escape rats both in the presence and absence of the phosphodiesterase inhibitor IBMX. By immunoblotting, we show that the abundance of two proteins important in cAMP generation: the stimulatory heterotrimeric G protein subunit Gsalpha and adenylyl cyclase type VI, do not change. We conclude that vasopressin escape is associated with relative vasopressin resistance of the collecting duct cells manifested by decreased intracellular cAMP levels. The decreased cAMP levels can contribute to the demonstrated decrease in collecting duct water permeability in two ways: 1) by causing a decrease in aquaporin-2 expression and 2) by limiting the acute action of vasopressin to increase collecting duct water permeability.

antidiuretic hormone; aquaporin-2; adenosine 3',5'-cyclic monophosphate; osmotic water permeability; urinary concentrating mechanism


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