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Modulatory effect of cyclic AMP on calcium fluxes in FRTL‐5 cells
Author(s) -
Törnquist Kid,
Ahlström Mikael
Publication year - 1993
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041570323
Subject(s) - thapsigargin , forskolin , calcium , endocrinology , chemistry , medicine , calcium atpase , phosphodiesterase inhibitor , ibmx , agonist , atpase , biology , receptor , biochemistry , enzyme
The aim of the present study was to investigate the effect of cAMP on calcium fluxes in Fura 2 loaded thyroid FRTL‐5 cells. Preincubating the cells with the phosphodiesterase inhibitor Ro‐201724 decreased the ATP‐stimulated entry of calcium, while having no effect on the release of sequestered calcium. Pretreatment with forskolin decreased both the release of sequestered calcium and the entry of calcium in response to ATP. We then incubated the cells with phenylisopropyl adenosine (PIA), a P 21 ‐receptor agonist earlier shown to decrease cAMP in FRTL‐5 cells. Although we did not observe a decrease in cellular cAMP after PIA, the ATP‐evoked calcium response was enhanced. Forskolin decreased calcium entry induced by thapsigargin a Ca 2− ‐ATPase inhibitor, but forskolin had no effect on the thapsigargin‐evoked release of sequestered calcium. Addition of calcium to cells stimulated with ATP in a calcium‐free buffered resulted in a rapid influx of calcium. This response in [Ca 2+ ] i was decreased in cells pretreated with forskolin. In cells stimulated with thapsigargin, the increase in [Ca 2+ ] i after addition of calcium was inhibited in part by forskolin and enhanced by PIA. The results suggest that cAMP may regulate calcium fluxes in FRTL‐5 cells Furthermore, PIA increased agonist‐induced calcium entry through a presently unknown mechanism. © 1993 Wiley‐Liss, Inc.