Abstract
Female rats were treated in vivo with estrogen for three weeks. The pituitaries were then removed and their responses to somatostatin, dopamine, TRH, hGHRH(1-44)NH2, or their combination were examined in a superfused pituitary cell system. Somatostatin did not decrease basal prolactin secretion in the control cells, but it caused a dose-dependent decrease in prolactin release from the estrogen pretreated cells. Estrogen pretreatment did not alter the sensitivity of pituitary cells to dopamine; dopamine was equally effective in the control and estrogen pretreated pituitaries in decreasing the basal prolactin secretion and TRH induced prolactin release. Prolactin release from the estrogen pretreated cells, stimulated by 25 nM TRH was inhibited by 1 nM somatostatin and nearly totally abolished by 25 nM somatostatin, whereas in the control cells only the higher dose of somatostatin caused some decrease in the prolactin release. Estrogen pretreated cells showed a reduced response to GHRH. Somatostatin did not decrease the basal secretion of GH in either group, but at 1 nM dose it completely abolished the GH release induced by equimolar concentration of GHRH. However, after somatostatin was eliminated from the system, a delayed GH release could be observed that was greater in the control pituitaries than in the estrogen pretreated pituitaries. It is concluded that in vivo treatment with estrogen reduces GH secretion in response to GHRH and increases prolactin secretion after TRH stimulation. After estrogen treatment, the basal and TRH stimulated prolactin release can be effectively reduced by somatostatin. These effects could be observed in vitro using estrogen free tissue culture medium for up to 36 hours after the removal of the pituitaries. The reciprocal changes in GH and prolactin secretion support the concept of the transdifferentiation of GH and prolactin secreting cells.
