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Am J Physiol Renal Physiol 296: F355-F361, 2009. First published November 5, 2008; doi:10.1152/ajprenal.90426.2008
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Signaling pathways utilized by PTH and dopamine to inhibit phosphate transport in mouse renal proximal tubule cells

Rochelle Cunningham,1 Rajatsubhra Biswas,1 Marc Brazie,1 Deborah Steplock,1 Shirish Shenolikar,4 and Edward J. Weinman1,2,3

Departments of 1Medicine and 2Physiology, University of Maryland School of Medicine and Medical Service, 3Department of Veterans Affairs Medical Center, Baltimore, Maryland; and 4Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, North Carolina

Submitted 21 July 2008 ; accepted in final form 31 October 2008

The present experiments were designed to detail factors regulating phosphate transport in cultured mouse proximal tubule cells by determining the response to parathyroid hormone (PTH), dopamine, and second messenger agonists and inhibitors. Both PTH and dopamine inhibited phosphate transport by over 30%. The inhibitory effect of PTH was completely abolished in the presence of chelerythrine, a PKC inhibitor, but not by Rp-cAMP, a PKA inhibitor. By contrast, both chelerythrine and Rp-cAMP blocked the inhibitory effect of dopamine. Chelerythrine inhibited PTH-mediated cAMP accumulation but also blocked the inhibitory effect of 8-bromo-cAMP on phosphate transport. On the other hand, Rp-cAMP had no effect on the ability of DOG, a PKC activator, to inhibit phosphate transport. PD98059, an inhibitor of MAPK, had no effect on PTH- or dopamine-mediated inhibition of sodium-phosphate cotransport. Finally, compared with 8-bromo-cAMP, 8-pCPT-2'-O-Me-cAMP, an activator of EPAC, had no effect on phosphate transport. These results outline significant differences in the signaling pathways utilized by PTH and dopamine to inhibit renal phosphate transport. Our results also suggest that activation of MAPK is not critically involved in PTH- or dopamine-mediated inhibition of phosphate transport in mouse renal proximal tubule cells in culture.

parathyroid hormone; PKA; PKC


Address for reprint requests and other correspondence: R. Cunningham, Dept. of Medicine, Division of Nephrology, Univ. of Maryland, School of Medicine, Rm. N3W143, UHM, 22 South Greene St., Baltimore, MD 21201 (e-mail: rcunning{at}medicine.umaryland.edu)




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