Effects of supraphysiological concentrations of progesterone on the characteristics of the oestradiolinduced gonadotrophin surge in women

Abstract

Intramuscular injections of oestradiol benzoate were given to 8 normally cyclic women in the early follicular phase of 3 different cycles. Progesterone was also injected in the second (low dose) and the third cycle (high dose). Oestradiol induced simultaneous surges of LH and FSH in all women and the onset of these surges was advanced by progesterone. Low-dose progesterone induced a significant increase in the amplitude and the duration of the LH and FSH surges, while high-dose progesterone decreased the duration significantly. In contrast to the oestrogen-only treatment cycles, when the women were treated with progesterone, basal LH and FSH concentrations were suppressed significantly not only before the onset but also after the end of the surge. The results suggest that progesterone affects the dimension of the oestradiol-induced gonadotrophin surge by exerting both a stimulatory and an inhibitory effect on pituitary gonadotrophin secretion. Supraphysiological concentrations of progesterone decreased the duration of the oestradiol-induced gonadotrophin surge significantly and this is possibly part of the mechanism which attenuates the endogenous LH surge in women superovulated for in-vitro fertilization.

Phytoestrogens enhance antioxidant enzymes after swimming exercise and modulate sex hormone plasma levels in female swimmers

“…The synthesis of estradiol is carried by the enzyme aromatase and regulated by negative feedback by estradiol itself, which inhibits pituitary FSH secretion by regulating GnRH and its receptor levels at the hypothalamus-pituitary level (Conn 1994;Braden and Conn 1993;Marshall et al 1983). Several studies have demonstrated the ability of exogenous estrogens to suppress FSH and LH levels during the follicular phase of the menstrual cycle (Tsai and Yen 1971;Monroe et al 1972;Young and Jaffe 1976;Messinis and Templeton 1990). By acting as an estrogenic agonist, verbascoside could act by inhibiting estradiol synthesis.…”

Evidence That Termination of the Estradiol-Induced Luteinizing Hormone Surge in Women Is Regulated by Ovarian Factors

“…It has also been shown that in ovariectomized and adrenalectomized rats treated with trilostane, estrogen-induced neuroprogesterone synthesis in hypothalamus is vital for the expression of the LH surge (22). On the other hand, after the exogenous administration of progesterone increasing values of this hormone facilitate the return of LH to the presurge level in a surge induced by exogenous estrogen (6). It is likely, therefore, that endogenous progesterone is important for the control of not only the onset (23) but also the amplitude of the midcycle LH surge partly via a contribution of rising progesterone values to the termination of the surge.…”

“…Several studies have reproduced the triggering effect of E2 on LH secretion in experiments performed either during the follicular phase of the menstrual cycle or in postmenopausal women (1)(2)(3)(4)(5)(6). Progesterone alone is unable to express a positive feedback effect unless its administration is preceded by estrogen treatment (7,8).…”

“…Progesterone alone is unable to express a positive feedback effect unless its administration is preceded by estrogen treatment (7,8). In such cases, progesterone advances the onset and enhances the amplitude of the E2-induced LH surge (4,6). It is likely that progesterone sensitizes the pituitary to GnRH because administration of the antiprogestagen mifepristone to normal women during the follicular phase of the cycle results in a reduction in the pituitary response to GnRH (9).…”

“…Exhaustion of the pituitary reserves is a possibility, but this has not been investigated. Another possibility is that the increasing progesterone values after the onset of the LH surge at midcycle may contribute to the surge termination, according to experiments in women including the exogenous administration of gonadal steroids (6). Nevertheless, the role of endogenous steroids has not been studied.…”