DYNAMICS OF PROLACTIN SECRETION FROM DIETHYLSTILBESTROL-INDUCED RAT PROLACTINOMA TISSUE IN-VITRO

Experiments were performed to determine whether PRL secretion in the r at diethylstilbestrol (DES)-induced prolactinoma model is affected by the addition of thyrotropin-releasing hormone (TRH) and/or immunoneutr alization of Intrapituitary vasoactive intestinal polypeptide (VIP) in vitro. Male Fischer 344 rats were implanted with either a 10 mg DES o r placebo pellet 30 days prior to obtaining the anterior pituitary gla nds for perifusion. The anterior pituitaries were quartered and used i n three different perifusion experiments. In Experiment I, placebo-tre ated tissue channels were perifused for 2 baseline hr followed consecu tively by a 30-min exposure to 1:100 nonimmune rabbit serum (NRS), a 3 0-min wash, and a final 30-min exposure to 10(-5) M TRH. Additional pl acebo channels were run as above except 1:100 VIP antiserum (AVIP) was substituted for NRS and AVIP was added to the TRH. In Experiment II, the same perifusion protocol was used as in Experiment I, except DES-i nduced tumor tissue was used instead of placebo tissue. Results from E xperiment I and II reveal that AVIP significantly decreased PRL secret ory rate in both DES and placebo groups. In the tumor group, both TRH alone and in the presence of AVIP significantly increased the PRL secr etory rate. In Experiment III DES-induced tumor tissue channels were p erifused with a similar protocol, except the concentrations of NRS and AVIP were increased to 1:10. Both NRS and AVIP significantly decrease d PRL secretory rate; however, AVIP had a significantly greater effect than NRS. In this experiment, 1:10 AVIP overcame the stimulatory effe ct of TRH. In conclusion, AVIP decreases and TRH increases, even in th e presence of AVIP, PRL release in DES-induced prolactinoma tissue in vitro. Increasing the AVIP concentration IO-fold diminished the PRL-re leasing action of TRH in the tumor tissue. These data suggest that PRL secretion is not autonomous in these prolactinomas and can be affecte d by exogenous TRH and partial immunoneutralization of endogenous VIP.