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,
PAOLO FILIPPONI,
LEONE FEDELI,
RENATO PALUMBO,
PIERANGELO SANTORI,
FAUSTO SANTEUSANIOI and
PAOLO BRUNETTI
Institutes of Clinical Medicine and Medical Pathology 06100 Perugia, Italy
the Center of Nuclear Medicine, Perugia University School of Medicine 06100 Perugia, Italy
Address all correspondence and requests for reprints to: Prof. Paolo Brunetti, Istituto di Patologia Medica Universita, Policlinico Monteluce, 06100 Perugia, Italy.
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 bromocriptinepretreated 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.
* Presented in part at the International Symposium on The Menopause: Clinical, Endocrinological and Pathophysiological Aspects, Viareggio, Italy, 1980. This work was supported in part by Italian C.N.R. Grant 79.01851.04
Recipient of a fellowship by Italian Ministry of Health.
Received October 1, 1980.
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