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Interactions of Estradiol and Progesterone on Pituitary Gonadotropin Secretion: Possible Sites and Mechanisms of Action
Ist Teil von
Biology of reproduction, 1979-06, Vol.20 (5), p.1173-1185
Ort / Verlag
United States: Society for the Study of Reproduction
Erscheinungsjahr
1979
Quelle
MEDLINE
Beschreibungen/Notizen
The effects of estradiol (E 2 ) alone or with progesterone (P) on spontaneous or LHRH-induced
releases of LH/FSH were examined 14-19 days after ovariectomy of rats. At 14 days, a Silastic E 2
capsule was implanted s.c. (Day 0) and 72 h later (Day 3) 2 groups of rats received either sesame
oil or progesterone (2 mg) s.c. Hourly blood samples were collected sequentially from 1200-1800
h on Day 3 and again at 0900 h and 1600 h on Days 4 and 5 (96 and 120 h post E 2 ). Control
groups included proestrous and untreated ovariectomized rats. Based on the data obtained we
concluded that: a) Daily LH but not necessarily FSH surges occur on Days 2, 3, 4 and 5 but not
on the day following E 2 treatment (Day 1). b) The responsiveness of the pituitary gland to 250 ng
LHRH is equal in both E 2 -treated (Day 3) and proestrous rats. However, the magnitude of the
spontaneous LH surge in E 2 -treated rats (Day 3), was 60% less than in normal proestrous animals.
Thus, E 2 seems to reduce the amount of endogenous LHRH released on Day 3. c) Progesterone,
given at 0900 h to E 2 -treated rats (Day 3), resulted in afternoon LH and FSH surges that were
earlier in their onset and of greater magnitude than those in E 2 -treated or normal proestrous rats.
However, no plasma LH increases occurred in E 2 P-treated rats on Days 4 and 5 unlike in rats
receiving only E 2 ; d) If spontaneous LH surges were blocked with Nembutal on Day 3, the magnitude of the LH surge on Day 4 in E 2 -treated rats was 2-fold greater than that observed on Day 4 in
rats which spontaneously released LH on Day 3. E 2 P-treated rats which received Nembutal on Day
3 also had spontaneous LH surges on Day 4 which were less in concentration than those of E 2 -treated animals on Day 4 or those obtained at 1600 h on Day 3 in the E 2 P-treated group. e)
Pituitary gland responsiveness to LHRH in E 2 P-treated rats is equal to that of E 2 -treated rats on
Day 3. The responsiveness of the pituitary gland on Day 4 in E 2 P-treated rats is significantly less
than that in E 2 -treated rats on Day 4; however, it is equal to the responsiveness found on Day 3 in
E 2 P-treated rats. Therefore, the stimulatory effect of P appears to be due to an increased release
of endogenous LHRH. The failure of LH/FSH surges to occur on Day 4 in E 2 P-treated rats may
not be due to the loss of 24 h periodicity in the intrinsic neural signal or to a severe decline in the
releasable LH pituitary pool. Rather it could be due to the failure of the hypothalamus to discharge sufficient LHRH to evoke
LH/FSH surges presumably because of inadequate releasable
LHRH reserves.