Horm Metab Res 1988; 20(1): 44-48
DOI: 10.1055/s-2007-1010745
Clinical

© Georg Thieme Verlag, Stuttgart · New York

Catecholamines and Pituitary Function. VII: Effects of Acute and Chronic Dopamine-Receptor Blockade on Pituitary Response to TRH-GNRH in Normal Women and in Patients with Hyperprolactinemic Amenorrhea

C. Giammartino2 , F. Ambrosi2 , G. Pelicci2 , M. C. Pagliacci2 , L. Fedeli1 , I. Nicoletti2
  • 1Centro di Medicina Nucleare, Università di Perugia, Perugia, Italy
  • 2Istituto di Clinica Medica 1, Università di Perugia, Perugia, Italy
Further Information

Publication History

1986

1987

Publication Date:
14 March 2008 (online)

Summary

To investigate whether an enhanced dopamine (DA) inhibition on pituitary thyrotrophs and gonadotrophs may account for the abnormal TSH and LH dynamics in pathological hyperprolactinemia, we examined the effect of an acute lysis of the putative DA overinhibition, as obtained with continuous domperidone (DOM) infusion, on both basal and TRH-GnRH stimulated PRL, TSH and LH release in both normal cycling women and patients with pathological hyperprolactinemia. The effect of TRH-GnRH administration was also examined in women with DA-antagonist induced hyperprolactinemia, in order to evaluate the effect of a chronic lack of the physiological DA inhibition on pituitary hormone dynamics.

Patients with both pathological and DA-antagonist induced hyperprolactinemia displayed an evident TSH and LH hyperresponsiveness to TRH-GnRH. The PRL response was reduced in the former but enhanced in the latter group. Domperidone infusion resulted in a marked increase in serum PRL levels in normal cycling women, but not in patients with pathological hyperprolactinemia. The abolition of the putative DA-overinhibition at the pituitary level with DOM infusion in patients with pathological hyperprolactinemia was followed by a slight increase in basal TSH output but did not modify the TSH and LH hyperresponsiveness to TRH-GnRH.

The similarities in TSH and LH dynamics between patients with pathological and DA-antagonist induced hyperprolactinemia and the ineffectiveness of DOM infusion in modifying the TSH and LH hyperresponses to TRH-GnRH in the former group, seem to exclude the widely accepted idea that endogenous DA overactivity is responsible for the abnormal thyrotroph and lactotroph dynamics in women with hyperprolactinemic amenorrhea.