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JOHN R. PEPPERELL, SANDRA L. PRESTON, HAROLD R. BEHRMAN, The Antigonadotropic Action of Prostaglandin F2α Is not Mediated by Elevated Cytosolic Calcium Levels in Rat Luteal Cells, Endocrinology, Volume 125, Issue 1, 1 July 1989, Pages 144–151, https://doi.org/10.1210/endo-125-1-144
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Abstract
We have investigated the role of intracellular calcium in the mechanism of action of prostaglandin F2α (PGF2α) in cultured rat luteal cells. PGF2α (1 μM) maximally inhibited LH-stimulated cAMP accumulation and also initiated a transient release of intracellular calcium. Low doses of the calcium ionophore ionomycin also increased intracellular calcium to a similar extent as PGF2α (1 μM), but did not inhibit LH-stimulated cAMP accumulation.
Chelation of intracellular calcium with dimethyl bis-(o-aminophenoxy) ethane-N,N,N′,N′-tetraacetic acid (BAPTA) (10 μM) attenuated the transient calcium rise stimulated by PGF2α, but did not affect the inhibitory characteristics of PGF2α on LHstimulated cAMP accumulation.
Treatment of luteal cells with EGTA (1 mM) and ionomycin (500 nM) resulted in depletion of intracellular calcium to such an extent that a subsequent exposure of the luteal cells to PGF2α (1 μM) did not elicit any change in intracellular calcium. Depletion of intracellular calcium and ablation of the calcium response to PGF2α, however, did not affect either the dose response or the time course of inhibition of LH-stimulated cAMP accumulation.
We conclude that although intracellular calcium is mobilized by PGF2α in cultured rat luteal cells, the antigonadotropic action of PGF2α on LH-stimulated cAMP accumulation is not mediated by this mechanism.