Progesterone Positive Feedback on Gonadotropin Release in Estrogen-Primed Postmenopausal Women: Central Nervous System and Pituitary as Possible Sites of Action*

Abstract

To investigate the site and mode of action of progesterone in inducing gonadotropin release, the effects of catecholamine-depleting (methyldopa) or dopamine agonist (bromocriptine) drugs on progesterone positive feedback and the gonadotropin response to a centrally acting noradrenergic drug (clonidine) were evaluated in estrogen-primed postmenopausal women. Progesterone administration induced a significant rise in LH, FSH, and PRL serum levels in the control group. Bromocriptine administration was followed by a marked suppression of PRL release but did not modify the gonadotropin response to progesterone. Methyldopa pretreatment significantly reduced the progesterone-induced LH surge, while PRL release was unaffected. After estrogen priming, clonidine administration did not result in an increase in serum LH or FSH concentrations. The dissociated responses of LH and PRL in bromocriptine-pretreated subjects and the significant reduction of the LH rise after progesterone in methyldopa-pretreated women seem to invalidate the hypothesis that a fall in endogenous dopamine is responsible for progesterone positive feedback and suggest that neural noradrenergic mechanisms are involved in progesterone-induced gonadotropin release. The ineffectiveness of a centrally acting noradrenergic agonist in inducing gonadotropin rise provides indirect evidence that an increased pituitary responsiveness may also be involved in progesterone positive feedback.

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

“…Hormone assay and analysis of data Serum T3, T4 and Prl were measured bv specific radioimmunoassavs as previously described (Nicoletti et al 1981). Thvroglobiilin and thvroid-microsomal anti¬ bodies were evaluated by commercial haemagglutination tests (Thymune M and Thymune T, Wellcome, Beckenham, England).…”

Catecholamines and Pituitary Function

“…Our data do not agree, therefore, with the conclusions by Quigley et al [21] who observed LH release after DA-antagonist administration in women with prolacti noma. Although it is possible that the con current inhibition of norepinephrine synthe sis induced by AMPT [36,37] is responsible for the lack of gonadotropin response to the fall in DA neurotransmission in our subjects, since it has been demonstrated that nor adrenergic pathways stimulate gonadotropin secretion in both animal models [41][42][43] and humans [44], it must be underlined that neither Elli et al [35] nor Ambrosi et al [22] were able to show significant rises in serum LH after sulpiride or metoclopramide ad ministration in hyperprolactinemic patients. These and our data seem to negate, therefore, the possibility that DA hyperactivity in the hypothalamus inhibits gonadotropin secre tion in hyperprolactinemia.…”

“…This seems to represent further proof against the hypothesis that DA hyperactivity at the Gn-RH-secreting terminals in the median eminence accounts for the impaired go nadotropin dynamics in hyperprolactinemic states. The lack of variations in gonadotropin concentrations during EPI infusion does not question, on the other hand, the possibility that adrenergic neurons are involved, at higher levels, in the control of gonadotropin release [41][42][43][44]54], since EPI does not cross the blood-brain barrier.…”

EFFECTS OF CLONIDINE ON POLYPEPTIDE AND STEROID HORMONE LEVELS IN MAN: A review

“…Increased GH secretion is a well known endocrine consequence of clonidine administration in healthy individuals (3, 4, 5, 6,8,9,10,11,12,13,14). Thus intravenous or oral administration of 150-300 pg clonidine raises peripheral GH levels to a peak value 6-10 times higher than the pretreatment level after 50-90 min, depending upon the mode of administra-Key words: Clonidine, steroid hormones, peptide hormones, man tion (3, 4,9,11,12).…”