Journal of Clinical Endocrinology & Metabolism, Vol 53, 135-138, Copyright © 1981 by Endocrine Society
Progesterone positive feedback on gonadotropin release in estrogen- primed postmenopausal women: central nervous system and pituitary as possible sites of action
I Nicoletti, P Filipponi, L Fedeli, R Palumbo, P Santori, F Santeusanio and P Brunetti
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.
