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Am J Physiol Renal Physiol 282: F324-F329, 2002. First published October 10, 2001; doi:10.1152/ajprenal.00251.2001
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Vol. 282, Issue 2, F324-F329, February 2002

Novel regulation of cell [Na+] in macula densa cells: apical Na+ recycling by H-K-ATPase

János Peti-Peterdi1, Zsuzsa Bebok2, Jean-Yves Lapointe3, and P. Darwin Bell1

1 Nephrology Research and Training Center, Division of Nephrology, and 2 Division of Hematology and Oncology, Department of Medicine and Physiology, and Gregory Flaming James Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, Alabama 35294; and 3 Membrane Transport Research Group, University of Montreal, Montreal, Quebec, Canada H3C 3J7

Na-K-ATPase is the nearly ubiquitous enzyme that maintains low-Na+, high-K+ concentrations in cells by actively extruding Na+ in exchange for K+. The prevailing paradigm in polarized absorbing epithelial cells, including renal nephron segments and intestine, has been that Na-K-ATPase is restricted to the basolateral membrane domain, where it plays a prominent role in Na+ absorption. We have found, however, that macula densa (MD) cells lack functionally and immunologically detectable amounts of Na-K-ATPase protein. In fact, these cells appear to regulate their cytosolic [Na+] via another member of the P-type ATPase family, the colonic form of H-K-ATPase, which is located at the apical membrane in these cells. We now report that this constitutively expressed apical MD colonic H-K-ATPase can function as a Na(H)-K-ATPase and regulate cytosolic [Na+] in a novel manner. This apical Na+-recycling mechanism may be important as part of the sensor function of MD cells and represents a new paradigm in cell [Na+] regulation.

macula densa; sodium-potassium-5'-adenosinetriphosphatase; colonic hydrogen-potassium-5'-adenosinetriphosphatase; sodium-binding benzofuran isophthalate


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