Evidence that chorion-decidual prolactin release is calcium dependent.
The regulation of PRL release from chorion-decidual explants was evaluated in organ cultures. Agents previously shown to stimulate pituitary release in vitro (TRH, theophylline, estradiol, and vasoactive intestinal polypeptide) were all without effect on chorion-decidual PRL release. Media free of calcium, however, resulted in 44% decreased chorion-decidual PRL release. Conversely, 2.5 mM CaCl2 produced a 64% increase in PRL release (P less than 0.01). Also, calcium chelation with EGTA (0.125-1.0 mM) produced a dose-related decrease in chorion-decidual PRL release. This decrease was greatest at 1.0 mM (P less than 0.01), being 56% of control. In contrast, the calcium-calmodulin complex inhibitor trifluoperazine (10 micrometers) did not significantly alter chorion-decidual PRL release. These studies and previous report in the literature suggest that different control mechanisms govern pituitary and chorion-decidual PRL release; however, an exception appears to be a common role for calcium.
D002118:Calcium / Q000378:metabolism*; D002823:Chorion / Q000187:drug effects / Q000378:metabolism*; D003513:Cycloheximide / Q000494:pharmacology; D003656:Decidua / Q000187:drug effects / Q000378:metabolism*; D005260:Female; D006801:Humans; D009924:Organ Culture Techniques; D011247:Pregnancy; D011388:Prolactin / Q000378:metabolism*
D011388:Prolactin; D003513:Cycloheximide; D002118:Calcium