Positive Feedback Effect of Progesterone on Luteinizing Hormone (LH) Release in Cyclic Female Rhesus Monkeys: LH Response Occurs in Two Phases*

1980 ◽  
Vol 51 (6) ◽  
pp. 1245-1250 ◽  
Author(s):  
EI TERASAWA ◽  
JORGE F. RODRIGUEZ-SIERRA ◽  
DONALD J. DIERSCHKE ◽  
WILLIAM E. BRIDSON ◽  
ROBERT W. GOY
1981 ◽  
Vol 36 (6) ◽  
pp. 309-310
Author(s):  
El TERASAWA ◽  
JORGE F. RODRIGUEZ-SIERRA ◽  
DONALD J. DIERSCHKE ◽  
WILLIAM E. BRIDSON ◽  
ROBERT W. GOY

1970 ◽  
Vol 46 (1) ◽  
pp. 1-7 ◽  
Author(s):  
S. TALEISNIK ◽  
M. E. VELASCO ◽  
J. J. ASTRADA

SUMMARY The influence that the interruption of the neural afferents to the hypothalamus exerts on ovulation and on the release of luteinizing hormone (LH) was studied in the rat. Animals with retrochiasmatic sections interrupting the neural connexions between the medial hypothalamus and the preoptic area (POA) showed constant oestrus and failed to ovulate. Animals in which the dorsal neural afferents to the POA were transected had oestrous cycles and ovulated normally. The positive feedback effect of progesterone on LH release in spayed animals primed either with 20 μg. oestradiol benzoate or 2·5 mg. testosterone propionate 3 days before was studied. Transection of the dorsal afferents to the POA favoured an increase in plasma LH, but in animals with retrochiasmatic sections the response was abolished. However, the negative feedback effect of ovarian steroids operated after both types of transection because an increase in plasma LH occurred after ovariectomy. It is concluded that the negative feedback effect of ovarian steroids acts on the medial hypothalamus which can maintain a tonic release of gonadotrophins in the absence of steroids. In contrast, the POA involved in the positive feedback effect of progesterone is concerned with the phasic release of LH.


1980 ◽  
Vol 86 (3) ◽  
pp. 459-464 ◽  
Author(s):  
P. J. SHARP ◽  
R. MASSA

In the laying hen, progesterone was shown to be converted in vitro in the pituitary gland and the hypothalamus to 5β-pregnane-3,20-dione (5β-DHP), 5β-pregnan-3α-ol-20-one (5β,3α-ol) and 5α-pregnane-3,20-dione (5α-DHP) and in the hyperstriatum dorsale to 5β-DHP and 5β,3α-ol. The conversion of progesterone to 5β-reduced metabolites was greater in the hyperstriatum dorsale than in the hypothalamus (P<0·001) and greater in the hypothalamus than in the pituitary gland (P <0·01). The conversion of progesterone to 5β-reduced metabolites was greater than its conversion to 5α-DHP in the pituitary gland (P <0·01) and the hypothalamus (P < 0·001). The possibility was investigated that 5α-DHP and 5β-DHP may act as metabolic intermediaries in the mechanism by which progesterone exerts a positive feedback effect on LH release. Progesterone, 5α-DHP and 5β-DHP were injected into laying hens at doses of 0·05,0·25 and 1·25 mg/kg and the changes in the concentration of plasma LH were followed for 4 h thereafter. Secretion of LH was stimulated after treatment with progesterone or 5α-DHP but not 5β-DHP. Progesterone stimulated LH release more effectively than did 5α-DHP, since an increase in the concentration of plasma LH was observed after 0·25 mg progesterone/kg but not after the same dose of 5α-DHP. It was concluded that in the hen 5α-DHP is unlikely to play a role in the induction of the preovulatory release of LH.


1980 ◽  
Vol 33 (4) ◽  
pp. 465 ◽  
Author(s):  
PJ Wright ◽  
T Stelmasiak ◽  
WA Chamley

Oestradiol-17 p (40 fig intravenously) failed to elicit a surge in plasma LH levels by 13 h after administration in 64 % (16 out of 25) Merino ewes about 30 days post partum in the anoestrous season. LH-RH responsiveness and LH-RH priming effect were significantly greater in these ewes than in similar post-partum (n = 9) and non-parturient ewes (n = 3) not treated with oestradiol. This suggests that the failure of the oestrogen-positive feedback effect on LH release in post-partum ewes is not due to a failure of oestradiol action on the pituitary increasing pituitary responsiveness to LH-RH and LH-RH priming effect, but could be due to inadequate release of LH-RH from the hypothalamus.


1982 ◽  
Vol 100 (4) ◽  
pp. 492-498 ◽  
Author(s):  
Koji Koike ◽  
Toshihiro Aono ◽  
Hirohisa Tsutsumi ◽  
Akira Miyake ◽  
Keiichi Kurachi

Abstract. The effect of hyperprolactinaemia on the hypothalamo-pituitary axis was assessed by iv injection of 100 μg luteinizing hormone releasing hormone (LRH) in 7 women with prolactinoma before and 3 months after normalization of the Prl level by transsphenoidal surgery. A dose of 20 mg of conjugated oestrogen (Premarin®) was also injected iv into patients with prolactinoma before and 4 months after surgery, and the serum LH levels were determined serially for 120 h after the injection. Surgical treatment caused significant reduction of the mean (± se) serum prolactin (Prl) level from 123.3 ± 7.8 to 19.4 ± 5.6 ng/ml. But the differences in the basal levels of LH (11.3 ± 2.2 to 8.6 ± 1.5 mIU/ml), FSH (8.3 ± 2.4 to 10.6 ± 3.7 mIU/ml) and oestradiol (26.6 ± 8.6 to 37.5 ± 5.5 pg/ml) before and 4 months after surgery were not significant. An exaggerated LH response to LRH in untreated prolactinoma patients was also observed after surgical treatment. After surgical treatment, patients showed LH release with a peak between 48 and 72 h after the injection of Premarin, whereas before treatment they did not show any LH discharge. The mean percent increase in LH between 48 and 72 h was also significantly higher after operation than before operation. These results suggest that the hyperprolactinaemia in prolactinoma patients may cause an impaired positive feedback effect of oestrogen on LH release and that this derangement can be reversed by reduction of the Prl level by adenomectomy.


2018 ◽  
Vol 107 (2) ◽  
pp. 133-146 ◽  
Author(s):  
David H. Abbott ◽  
Sarah H. Vepraskas ◽  
Teresa H. Horton ◽  
Ei Terasawa ◽  
Jon E. Levine

Background/Aims: Ovarian theca cell hyperandrogenism in women with polycystic ovary syndrome (PCOS) is compounded by androgen receptor-mediated impairment of estradiol and progesterone negative feedback regulation of episodic luteinizing hormone (LH) release. The resultant LH hypersecretion, likely the product of accelerated episodic release of gonadotropin-releasing hormone (GnRH) from the median eminence of the hypothalamus, hyperstimulates ovarian theca cell steroidogenesis, enabling testosterone (T) and androstenedione excess. Prenatally androgenized (PA) female monkeys exposed to fetal male levels of T during early-to-mid gestation, when adult, demonstrate PCOS-like traits, including high T and LH levels. This study tests the hypothesis that progesterone resistance-associated acceleration in episodic LH release contributes to PA monkey LH excess. Methods: A total of 4 PA and 3 regularly cycling, healthy control adult female rhesus monkeys of comparable age and body mass index underwent (1) a 10 h, frequent intravenous sampling assessment for LH episodic release, immediately followed by (2) IV infusion of exogenous GnRH to quantify continuing pituitary LH responsiveness, and subsequently (3) an SC injection of a progesterone receptor antagonist, mifepristone, to examine LH responses to blockade of progesterone-mediated action. Results: Compared to controls, the relatively hyperandrogenic PA females exhibited ~100% increase (p = 0.037) in LH pulse frequency, positive correlation of LH pulse amplitude (p = 0.017) with androstenedione, ~100% greater increase (p = 0.034) in acute (0–10 min) LH responses to exogenous GnRH, and an absence (p = 0.008) of modest LH elevation following acute progesterone receptor blockade suggestive of diminished progesterone negative feedback. Conclusion: Such dysregulation of LH release in PCOS-like monkeys implicates impaired feedback control of episodic release of hypothalamic GnRH reminiscent of PCOS neuroendocrinopathy.


1983 ◽  
Vol 97 (3) ◽  
pp. 319-325 ◽  
Author(s):  
E. Aguilar ◽  
C. Fernández Galaz ◽  
M. D. Vaticón ◽  
A. Tejero ◽  
A. Oriol

Neonatally oestrogenized female rats showed hyperprolactinaemia (prolactin, 230 μg/l), normal LH levels and absence of a positive feedback effect of oestrogen on secretion of LH at 5 months of age. Bromocriptine treatment for 13 days (1 mg/kg per day) caused no changes in LH levels and prolactin levels decreased to normal values (33 μg/l). This decrease in prolactin concentration was not followed by the recovery of phasic LH response to oestrogens. The effectiveness of oestrogens to induce prolactin secretion was greater in the neonatally oestrogenized rats than in the control group. In both cases the effect diminished after bromocriptine treatment. These results indicate that hyperprolactinaemia is not the cause of the anovulatory state in oestrogenized rats and that neonatal treatment with oestrogens alters oestrogen–prolactin relations, probably involving dopamine.


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