Abstract

The aim of the present study was to investigate whether the Ca 2+-ATPase inhibitor cyclopiazonic acid (CPA) could empty intracellular Ca 2+ stores and activate Ca 2+ influx in thyroid FRTL-5 cells. Addition of CPA to Fura-2 loaded cells rapidly increased intracellular free Ca 2+ ([Ca 2+] i) which then stabilized at a new elevated steady state level. The initial increase was mainly dependent on the release of sequestered Ca 2+, but was decreased in Ca 2+-free buffer and in depolarized cells. The plateau phase was totally dependent on extracellular Ca 2+. Addition of Ca 2+ to cells exposed to CPA in Ca 2+-free buffer rapidly increased [Ca 2+] i. This influx was decreased in depolarized cells and inhibited by SKF 96365. Addition of CPA to cells prior to stimulating the cells with ATP totally abolished the ATP-induced increase in [Ca 2+] i. In Ca 2+-free buffer, addition of ATP prior to CPA decreased the response in [Ca 2+] i evoked by CPA. The results show that emptying intracellular Ca 2+ stores with CPA rapidly activates influx of Ca 2+ in FRTL-5 cells. Furthermore, ATP and CPA appear to release Ca 2+, at least in part, from the same intracellular Ca 2+ store in these cells.

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