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J Biol Chem, Vol. 274, Issue 16, 11289-11295, April 16, 1999

Dual Mechanisms of Regulation of Na/H Exchanger NHE-3 by Parathyroid Hormone in Rat Kidney

Lingzhi Fan, Michael R. Wiederkehr, Roberto Collazo, Huamin Wang^¶, Ladonna A. Crowder, and Orson W. Moe^¶

From the ^¶ Medical Service, Department of Veterans Affairs Medical Center and the  Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75225-8856

Parathyroid hormone (PTH) is a potent inhibitor of mammalian renal proximal tubule sodium absorption via suppression of the apical membrane Na/H exchanger (NHE-3). We examined the mechanisms by which PTH inhibits NHE-3 activity by giving an acute intravenous PTH bolus to parathyroidectomized rats. Parathyroidectomy per se increased apical membrane NHE-3 activity and antigen. Acute infusion of PTH caused a time-dependent decrease in NHE-3 activity as early as 30 min. Decrease in NHE-3 activity at 30 and 60 min was accompanied by increased NHE-3 phosphorylation. In contrast to the rapid changes in NHE-3 activity and phosphorylation, decrease in apical membrane NHE-3 antigen was not detectable until 4-12 h after the PTH bolus. The decrease in apical membrane NHE-3 occurred in the absence of changes in total renal cortical NHE-3 antigen. Pretreatment of the animals with the microtubule-disrupting agent colchicine blocked the PTH-induced decrease in apical NHE-3 antigen. We propose that PTH acutely cause a decrease in NHE-3 intrinsic transport activity possibly via a phosphorylation-dependent mechanism followed by a decrease in apical membrane NHE-3 antigen via changes in protein trafficking.

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