Abstract

We have investigated the role of intracellular calcium in the mechanism of action of prostaglandin F (PGF) in cultured rat luteal cells. PGF (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 PGF (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 PGF, but did not affect the inhibitory characteristics of PGF 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 PGF (1 μM) did not elicit any change in intracellular calcium. Depletion of intracellular calcium and ablation of the calcium response to PGF, 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 PGF in cultured rat luteal cells, the antigonadotropic action of PGF on LH-stimulated cAMP accumulation is not mediated by this mechanism.

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