Abstract
The objective of this study was to determine the influence of estradiol 17β and/or progesterone on gonadotropin secretion at the level of the pituitary. Female rats in which the hypothalamo hypophyseal connections had been permanently interrupted after castration served as the experimental model in which the effect of estradiol and/or progesterone on LH RH induced gonadotropin release was examined. In our experimental animals, LH secretion was readily activated by LH RH administration. LH release was greatly augmented by the prior administration of estradiol benzoate (1 μg/kg b.w./day). Progesterone (5 mg/day) in the absence of estradiol did not modify the 10 min response to LH RH but reduced the enhancement of LH secretion caused by estradiol pretreatment. Our findings suggest that estradiol potentiated the releasing effect of LH RH at the level of the gonadotroph, whereas progesterone interfered with the potentiation effect. Plasma levels of FSH were not significantly elevated above the basal value by the administration of LH RH alone, or in combination with estradiol and/or progresterone.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 233-241 |
| Number of pages | 9 |
| Journal | Neuroendocrinology |
| Volume | 18 |
| Issue number | 3 |
| State | Published - 1975 |
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ASJC Scopus subject areas
- Endocrinology
- Neuroscience(all)
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Potentiation of luteinizing hormone release by estradiol at the level of the pituitary. / Greeley, G. H.; Allen, M. B.; Mahesh, V. B.
In: Neuroendocrinology, Vol. 18, No. 3, 1975, p. 233-241.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Potentiation of luteinizing hormone release by estradiol at the level of the pituitary
AU - Greeley, G. H.
AU - Allen, M. B.
AU - Mahesh, V. B.
PY - 1975
Y1 - 1975
N2 - The objective of this study was to determine the influence of estradiol 17β and/or progesterone on gonadotropin secretion at the level of the pituitary. Female rats in which the hypothalamo hypophyseal connections had been permanently interrupted after castration served as the experimental model in which the effect of estradiol and/or progesterone on LH RH induced gonadotropin release was examined. In our experimental animals, LH secretion was readily activated by LH RH administration. LH release was greatly augmented by the prior administration of estradiol benzoate (1 μg/kg b.w./day). Progesterone (5 mg/day) in the absence of estradiol did not modify the 10 min response to LH RH but reduced the enhancement of LH secretion caused by estradiol pretreatment. Our findings suggest that estradiol potentiated the releasing effect of LH RH at the level of the gonadotroph, whereas progesterone interfered with the potentiation effect. Plasma levels of FSH were not significantly elevated above the basal value by the administration of LH RH alone, or in combination with estradiol and/or progresterone.
AB - The objective of this study was to determine the influence of estradiol 17β and/or progesterone on gonadotropin secretion at the level of the pituitary. Female rats in which the hypothalamo hypophyseal connections had been permanently interrupted after castration served as the experimental model in which the effect of estradiol and/or progesterone on LH RH induced gonadotropin release was examined. In our experimental animals, LH secretion was readily activated by LH RH administration. LH release was greatly augmented by the prior administration of estradiol benzoate (1 μg/kg b.w./day). Progesterone (5 mg/day) in the absence of estradiol did not modify the 10 min response to LH RH but reduced the enhancement of LH secretion caused by estradiol pretreatment. Our findings suggest that estradiol potentiated the releasing effect of LH RH at the level of the gonadotroph, whereas progesterone interfered with the potentiation effect. Plasma levels of FSH were not significantly elevated above the basal value by the administration of LH RH alone, or in combination with estradiol and/or progresterone.
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M3 - Article
C2 - 1103003
AN - SCOPUS:0016753241
VL - 18
SP - 233
EP - 241
JO - Neuroendocrinology
JF - Neuroendocrinology
SN - 0028-3835
IS - 3
ER -