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Articles in PresS, published online ahead of print October 10, 2001
Am J Physiol Renal Physiol, 10.1152/ajprenal.00251.2001
Submitted on August 15, 2001
Accepted on October 2, 2001
1 Dept. of Medicine, Div. of Nephrology, NRTC, University of Alabama at Birmingham, Birmingham, AL, USA
2 Dept. of Medicine, Div. of Hematology and Oncology, Cystic Fibrosis Research Center, University of Alabama at Birmingham, Birmingham, AL, USA
3 Membrane Transport Research Group, University of Montreal, Montreal, Quebec, Canada
* To whom correspondence should be addressed. E-mail: petjan{at}uab.edu.
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 in the sensor function of MD cells and represents a new paradigm in cell [Na+] regulation.
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