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Am J Physiol Renal Physiol 257: F967-F973, 1989;
0363-6127/89 $5.00
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AJP - Renal Physiology, Vol 257, Issue 6 967-F973, Copyright © 1989 by American Physiological Society

ARTICLES

Sodium-phosphate cotransport in OK cells: inhibition by PTH and "adaptation" to low phosphate

G. Quamme, J. Biber and H. Murer
Department of Medicine, University of British Columbia, Vancouver, Canada.

Sodium-phosphate (Na-Pi) cotransport is principally regulated by parathyroid hormone (PTH) and by the intrinsic ability to "adapt" to ambient phosphate concentration. In the present study, these two control mechanisms were examined in a cloned opossum kidney (OK) cell line. PTH inhibited Na-Pi cotransport, half-maximal inhibition at 5 x 10(-12) M, by fractionally similar amounts irrespective of the initial transport rates predetermined by "adaptation" to media phosphate concentration. At maximal concentrations of PTH (10(-8) M), the residual Na-Pi cotransport activity was higher in cells exposed to low-phosphate media. Cells preexposed to PTH (10(-8) M) or dibutyryl adenosine 3'-5'-cyclic monophosphate (DBcAMP) (10(-5) M) and forskolin (10(-5) M) increase transport (adaptation) by fractionally similar amounts as control cells for any given external phosphate concentration. The protein kinase C inhibitor, staurosporine, prevented PTH action but did not alter the ability to adapt Na-Pi cotransport in response to low media phosphate concentration. These data support the notion that regulation of Na-Pi cotransport by PTH and the adaptive response to available media phosphate concentration are distinct regulatory control mechanisms.


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