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Dopamine and TRH-induced prolactin secretion in pseudopregnant rats
G A Schuiling1, N Valkhof, H Moes
1Department of Obstetrics and Gynaecology, University of Groningen, The Netherlands.
Abstract:
The stimulatory effect of TRH on prolactin (Pr1) secretion by the anterior pituitary gland (APG) of the pseudopregnant (PSP) rat was studied in vivo and in vitro. TRH, 500 micrograms, did not increase Pr1 release during the Pr1 peaks which are generated daily between 01.00 and 12.00 for about 10 days (mean height of the peaks: 302 +/- 99 ng mL-1), nor did TRH induce Pr1 secretion during the phase of low (12 +/- 1 ng Pr1 mL-1) secretion (the "interphase", between 20.00 and 01.00 h). 25 mg/kg b.w. of the dopamine- (DA) release blocking drug, 1-hydroxy-3-amino-pyrrolidone-2 (HA 966) did not itself induce peaks of Pr1 during the interphase, but in 1 animal out of 6 which were treated with this dose of HA 966, TRH (500 micrograms) induced a peak of Pr1 with a height of 264 ng mL-1 x 100 mg HA 966/kg b.w. induced during the interphase peaks of Pr1 which were as high as spontaneous Pr1 peaks (343 +/- 95 ng mL-1). TRH increased these Pr1 peaks to 844 +/- 48 ng mL-1. Apparently, HA 966 not only lowers DA concentrations but also somehow increases the TRH-responsiveness of the lactotrophs. In vitro, the secretion of Pr1 by incubated pituitary glands was suppressed to the same extent by 5 x 10(-8) and 10(-6) M DA. TRH stimulated Pr1 secretion in the presence of 5 x 10(-8) M DA, but not in the presence of 10(-6) M DA or in the absence of DA. It is concluded that in vitro TRH acts as a physiological antagonist of DA. It is suggested that in vivo the effectivity of TRH as a Pr1-releasing factor may be modulated by DA and that this effect of DA is independent from its Pr1-release suppressing effect.