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J Biol Chem, Vol. 275, Issue 3, 1807-1813, January 21, 2000

Parathyroid Hormone Controls the Size of the Intracellular Ca²⁺ Stores Available to Receptors Linked to Inositol Trisphosphate Formation^*

Alison D. Short and Colin W. Taylor

From the Department of Pharmacology, Tennis Court Road, Cambridge, CB2 1QJ, United Kingdom

In HEK 293 cells stably expressing type 1 parathyroid (PTH) receptors, PTH stimulated release of intracellular Ca²⁺ stores in only 27% of cells, whereas 96% of cells responded to carbachol. However, in almost all cells PTH potentiated the response to carbachol by about 3-fold. Responses to carbachol did not desensitize, but only the first challenge in Ca²⁺-free medium caused an increase in [Ca²⁺]_i, indicating that the carbachol-sensitive Ca²⁺ stores had been emptied. Subsequent addition of PTH also failed to increase [Ca²⁺]_i, but when it was followed by carbachol there was a substantial increase in [Ca²⁺]_i. A similar potentiation was observed between ATP and PTH but not between carbachol and ATP. Intracellular heparin inhibited responses to carbachol and PTH, and pretreatment with ATP and carbachol abolished responses to PTH, suggesting that the effects of PTH involve inositol trisphosphate (IP₃) receptors. PTH neither stimulated detectable IP₃ formation nor affected the amount formed in response to ATP or carbachol. PTH stimulated cyclic AMP formation, but this was not the means whereby PTH potentiated Ca²⁺ signals. We suggest that PTH may regulate Ca²⁺ mobilization by facilitating translocation of Ca²⁺ between discrete intracellular stores and that it thereby regulates the size of the Ca²⁺ pool available to receptors linked to IP₃ formation.

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