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Articles in PresS, published online ahead of print March 26, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00365.2001
Submitted on December 13, 2001
Accepted on March 25, 2002
1 Department of Physiology, University of Zurich, Zurich, Zurich, Switzerland
2 Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA
3 Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
4 Center of Mineral Metabolism and Clinical Research, University of Texas Southwestern Medical Center, Dallas, Texas, USA; Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas, USA
5 Department of Physiology, University of Zurich, Zurich, Zurich, Switzerland; Renal Division, University Hospital of Zurich, Zurich, Zurich, Switzerland
* To whom correspondence should be addressed. E-mail: patrice.ambuehl{at}dim.usz.ch.
Insulin is an important regulator of renal salt and water excretion and hyperinsulinemia has been implicated to play a role in hypertension. One of the target proteins of insulin action in the kidney is the Na+/H+ exchanger NHE3, a principal Na+ transporter responsible for salt absorption in the mammalian proximal tubule. The molecular mechanisms involved in activation of NHE3 by insulin have not been studied so far. In opossum kidney cells (OK cells), insulin increased Na+/H+ exchange activity in a time- and concentration-dependent manner. This effect is due to activation of NHE3 as it persisted after pharmacological inhibition of NHE1 and NHE2. In the early phase of stimulation (2-12h), NHE3 activity was increased without changes in NHE3 protein and mRNA. At 24 h, enhanced NHE3 activity was accompanied by an increase in total and cell surface NHE3 protein, and NHE3 mRNA abundance. All the effects of insulin on NHE3 activity, protein and mRNA were amplified in the presence of hydrocortisone. These results suggest that insulin stimulates renal tubular NHE3 activity via a biphasic mechanism involving post-translational factors and an increase in NHE3 gene expression and the effects are dependent on the permissive action of hydrocortisone.
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