Swine granulosa-luteal cells incubated in Ca2+-deficient medium (5μM final Ca2+ concentration) for short time periods produced diminished quantities of progesterone in response to lutropin. Maximally stimulating effects of prostaglandin E2 and L-adrenaline were also impaired significantly. Diminished progesterone production could not be attributed to alterations in protein synthesis or cell viability. Under Ca2+-deprived conditions, the stimulatory action of cholera toxin, 3-isobutyl-1-methylxanthine and 8-bromo-cyclic AMP were also significantly impeded. Administration of a presumptive antagonist of transmembrane Ca2+ influx (verapamil) or of EGTA to chelate extracellular Ca2+, significantly decreased the total cellular content of Ca2+, and antagonized the actions of lutropin. Micromolar concentrations of trifluoperazine mimicked the suppressive effects of Ca2+ deprivation. Conversely, the bivalent-cation ionophore, ionophore A23187, significantly augmented the stimulation of progesterone production by lutropin. Thus the present observations implicate Ca2+ in the modulation of hormonally stimulated progesterone production in isolated ovarian cells, and suggest that Ca2+ may influence one or more processes distal to, or independent of, cyclic AMP generation. In addition, the susceptibility of progesterone biosynthesis to inhibition by trifluoperazine suggests a possible role for calmodulin in the ovary.
|Original language||English (US)|
|Number of pages||6|
|State||Published - 1982|
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