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Am J Physiol Renal Physiol 275: F818-F826, 1998;
0363-6127/98 $5.00
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Vol. 275, Issue 5, F818-F826, November 1998

A tyrosine-based signal regulates H-K-ATPase-mediated potassium reabsorption in the kidney

Tong Wang, Nathalie Courtois-Coutry, Gerhard Giebisch, and Michael J. Caplan

Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510

Isoforms of the H-K-ATPase participate in active K resorption in the renal collecting tubule. The cytoplasmic tail of the beta -subunit of the gastric H-K-ATPase includes a 4 amino acid motif which is highly homologous to tyrosine-based endocytosis signals. We have generated transgenic mice expressing an H-K-ATPase beta -subunit in which the tyrosine residue in this sequence has been mutated to alanine. Mice expressing the mutated protein manifest constitutive hypersecretion of gastric acid, demonstrating that the beta -subunit tyrosine-based motif is required for the regulated endocytosis of the H-K pump and hence the cessation of gastric acid output. To test the possibility that the tyrosine-based sequence in the tail of the H-K-ATPase beta -subunit plays a role in regulating the function of renal H-K-ATPases, we examined renal K clearance in normal and in transgenic mice. Blood pressure, urine volume, glomerular filtration rate (GFR), plasma Na, and Na excretion are similar in control and transgenic mice. However, plasma K concentrations are significantly higher in transgenic mice (4.76 ± 0.13 meq/l in transgenic and 4.12 ± 0.04 meq/l in control; n = 9, P < 0.05) and K excretion is lower in the transgenic animals (fractional excretion of K was 26.2 ± 3.62% in transgenic and 50.1 ± 4.78% in control; n = 9, P < 0.01). These data suggest that the tyrosine-based signal in the cytoplasmic tail of the H-K-ATPase beta -subunit functions in the kidney as it does in the stomach to internalize H-K pump and thus inactivate pump function. Its elimination may result in the constitutive presence of the pump at the cell surface and lead to excessive urinary K reabsorption.

ion pump; proton-potassium-adenosinetriphosphatase; potassium absorption; endocytosis; transgenic mouse


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