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Articles in PresS, published online ahead of print July 30, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00059.2002
Submitted on February 11, 2002
Accepted on July 26, 2002
1 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Physiology, Dongguk University, Kyungju, Korea, Republic of
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
3 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA
4 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.
Adrenocortical steroid hormones are importantly involved in the regulation of extracellular fluid volume. The present study was aimed to examine whether aldosterone and/or glucocorticoid regulates the abundance of AQP-3, -2, and -1 in rat kidney. In protocol 1, rats were adrenalectomized followed by aldosterone replacement, dexamethasone replacement, or combined aldosterone and dexamethasone replacement (rats had free access to water but received a fixed amount of food). Protocol 2 was identical to protocol 1 except all groups received fixed daily food and water intake. In both protocol 1 and 2, aldosterone deficiency was associated with increased FENa and severe hyperkalemia. Semiquantitative immunoblotting revealed that aldosterone deficiency was associated with a dramatic downregulation of AQP3 abundance. Consistent with this, immunocytochemistry and immunoelectron microscopy revealed a marked decrease of AQP3 labeling in the basolateral plasma membranes of collecting duct principal cells. In contrast, AQP1 and AQP2 abundance and distribution was unchanged. Glucocorticoid deficiency revealed no changes in AQP3, -2, or -1 abundances. In protocol 3, sodium restriction (to increase endogenous aldosterone levels) or exogenous aldosterone infusion to either Wistar rats or vasopressin-deficient Brattleboro rats was associated with a major increase in AQP3 abundance whereas no change in AQP2 abundance was seen. In protocol 4, aldosterone levels were clamped by infusion of aldosterone, while Na intake was altered from low to a high level. Under these circumstances, there were no changes in AQP3 or AQP2 abundance, although the level of the Na-Cl cotransporter was decreased. In conclusion the results uniformly demonstrate that aldosterone regulates AQP3 abundance independent of sodium intake. In contrast, changes in glucocorticoid levels in these models do not influence AQP3 or AQP2 abundance. Therefore in the collecting duct aldosterone may regulate, at least in part, AQP3 expression in addition to regulating Na+ and K+ transport.
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