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1 Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA
2 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA
3 Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA; Department of Physiology and Department of Veterans Affairs Medical Center, Medical Service, University of Maryland School of Medicine f Veterans Affairs Medical Center, Baltimore, MD, USA; Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA
* To whom correspondence should be addressed. E-mail: eweinman{at}medicine.umaryland.edu.
The present experiments using primary cultures from renal proximal tubule cells, examines two aspects of the regulation of sodium-dependent phosphate transport and membrane Npt2a expression by PTH. Sodium-dependent phosphate transport in proximal tubule cells from wild-type mice grown in normal phosphate media averaged 4.4 ± 0.5 nmol/ mg protein/10 min and was inhibited by 30.5 ± 8.6% by PTH (10-7 M). This was associated with a 32.7 ± 5.2% decrease in Npt2a expression in the plasma membrane. Proximal tubule cells from NHERF-1-/- mice had a lower rate of phosphate transport compared to wild-type cells and a significantly reduced inhibitory response to PTH. Wild-type cells incubated in a low phosphate media for 24 hrs had a higher rate of phosphate transport compared to wild-type cells grown in normal phosphate media but a significantly blunted inhibitory response to PTH. These data indicate a role for NHERF-1in mediating the membrane retrieval of Npt2a and the subsequent inhibition of phosphate transport in the renal proximal tubules. These studies also suggest that there is a blunted phosphaturic effect of PTH in cells adapted to a low phosphate media.
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