A previous study demonstrated that prostaglandin F2α(PGF2α) stimulates a transient increase in cytosolic free Ca2+levels ([Ca2+]i) in ovine large luteal cells. In the present study, the magnitude of the PGF2α(0.5 /μM)-induced calcium transient in Hanks’ medium (87 ± 2 nM increase above resting levels) was reduced (P < 0.05) but not completely eliminated in fura-2 loaded large luteal cells incubated in Ca2+-free or phosphate- and carbonate-free medium (10 ± 1 nM, 32 ± 6 nM, above resting levels; respectively). Preincubation for 2 min with 1 mM LaCls (calcium antagonist) eliminated the PGF2α-induced calcium transient. The inhibitory effect of PGF2αon secretion of progesterone was reduced in Ca2+-free medium or medium plus LaCU. Resting [Ca2+]ilevels and basal secretion of progesterone were both reduced (P < 0.05) in large cells incubated in Ca2+- free medium (27 ± 4 nM; 70 ± 6% control, respectively) or with 5 nM 5, 5’-dimethyl bis-(0-aminophenoxy)ethane-N, N, N’, N’- tetraacetic acid (40 ± 2 nM; 49 ± 1% control; respectively). In addition, secretion of progesterone was inhibited (P < 0.05) by conditions that increased (P < 0.05) [Ca2+]i; that is LaCl3([Ca2+]i, 120 ± 17 nM; progesterone, 82 ± 8% control) and PGF2” ([Ca2+]i, 102 ± 10 nM; progesterone, 82 ± 3% control). In small luteal cells, resting [Ca2+]ilevels and secretion of progesterone were reduced by incubation in Ca2+-free Hanks ([Ca2+]i, 28 ± 2 nM; progesterone, 71 ± 6% control), however, neither LaCU nor PGF2αincreased [Ca2+]ilevels or inhibited secretion of progesterone. The findings presented here provide evidence that extracellular as well as intracellular calcium contribute to the PGF2α- induced [Ca2+]itransient in large cells. Furthermore, whereas an adequate level of [Ca2+]iis required to support progesterone production in both small and large cells, optimal progesterone production in large cells depends upon an appropriate window of [Ca2+]i.
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