Catecholamines and pituitary function. IV. Effects of low-dose dopamine infusion and long-term bromocriptine treatment on the abnormal thyrotroph (TSH) dynamics in patients with pathological hyperprolactinaemia
Abstract. In order to gain further insight into the role of dopamine (DA) in the control of TSH release and to investigate whether an increased or defective DA inhibition on pituitary thyrotrophs may be considered responsible for the abnormal TSH dynamics in pathological hyperprolactinaemia, we examined the effect of low-dose DA infusion on TRH stimulated TSH secretion in normally cycling women and in patients with pathological hyperprolactinaemia. The effect of long-term bromocriptine therapy on TSH dynamics was also evaluated in a selected group of hyperprolactinaemic women. Fifty-two hyperprolactinaemic patients with no other signs of pituitary or thyroid dysfunction had significantly higher mean TSH serum concentrations and mean TSH peak values after TRH administration than 75 healthy controls. Furthermore, the TSH rises induced by the DA-synthesis inhibitor α-methyl-p-tyrosine (AMPT, 500 mg orally) were enhanced in both prolactinoma and 'idiopathic hyperprolactinaemia' patients as compared with controls. There was a positive correlation between the TRH- and AMPT-induced TSH rises in the hyperprolactinaemic group. Low-dose DA infusion (0.1 μg/kg min) reduced TSH response to TRH in both regularly cycling women and patients with hyperprolactinaemic amenorrhoea. Long-term bromocriptine therapy (2.5 mg tid over 60– 150 days) not only normalized serum Prl levels, but also reduced the TSH response to TRH in 7 hyperprolactinaemic women who had presented exaggerated TSH responses to the basal TRH test. These findings confirm that DA plays a physiological role in the inhibition of TSH release, probably at the level of the anterior pituitary. The fact that both low-dose DA infusion and long-term bromocriptine treatment effectively reduced TSH release in hyperprolactinaemic patients seems to indicate that endogenous DA inhibition of pituitary thyrotrophs is reduced rather than enhanced in pathological hyperprolactinaemia.