PGE1 or PGE2 injected iv at different doses (5, 20 or 50 μg/100 g body wt) in ovariectomized rats failed to modify plasma prolactin levels 20, 60 or 90 min after injection. The diluent (95% ethanol) was also ineffective. Third ventricular injection of PGE1 (5 μg in 5 μl 95% ethanol: 0.02% Na2CO3, 1:9) in ovariectomized rats induced a marked increase in plasma prolactin levels 15 min later. Levels then declined but were still elevated at 30 min. At 60 min they were not different from the initial values. PGE2, PGFlα or PGF2α at the same dose failed to modify plasma prolactin at any time interval studied. The diluent also did not alter plasma prolactin. Intraventricular injection of different doses of PGE1 (0.5, 1.0, 2.5 or 5.0 μg in 5 μl) induced a dose-related increase of plasma prolactin 15 min after the injection. In ovariectomized, estrogen-treated rats (estradiol benzoate, Eb, 10 μg, SC, 48 hr before), PGE1 increased plasma prolactin 15 min later, in spite of the elevated initial plasma prolactin levels induced by the estrogen treatment. PGE2, PGFlα) PGF2α or the diluent were again ineffective. Intrapituitary injection of PGE1 (2.5 μg in 2.5 μl into each lobe) in ovariectomized rats slightly increased plasma prolactin levels at 15 min (p < 0.05). Similar injections of PGE2 did not alter plasma prolactin at any time interval studied. Intrapituitary injections of PGE1 or PGE2 in ovariectomized estrogen-treated rats at the same dose used before failed to increase plasma prolactin. These results indicate that PGE1 can stimulate prolactin release by acting on the central nervous system and that this effect is not inhibited by estrogen treatment. PGE2, PGF1α and PGF2α appear to be ineffective. Under certain conditions, PGE1 may also stimulate prolactin release by acting on the adenohypophysis, but this effect was inhibited by estrogen pretreatment.
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