Effect of progesterone on plasma luteinizing hormone activity

1962 ◽  
Vol 202 (4) ◽  
pp. 601-604 ◽  
Author(s):  
S. M. McCann
Keyword(s):  
Luteinizing Hormone ◽  
Marked Decrease ◽  
Estradiol Benzoate ◽  
Inhibitory Effect ◽  
Rat Plasma ◽  
Ovariectomized Rats ◽  
Ovariectomized Rat ◽  
Hormone Activity ◽  
Subcutaneous Injections ◽  
Plasma Pretreatment

The luteinizing hormone (LH) activity of ovariectomized rat plasma was estimated by the ovarian ascorbic acid depletion technique. A single subcutaneous injection of 25 mg of progesterone produced a slight decrease in this LH activity which was first demonstrable 2 days after injection of progesterone. If a second injection of 25 mg of progesterone was given 2 days after the first, a marked decrease in LH activity was found on testing a day later. Three daily subcutaneous injections of 5 mg of progesterone failed to significantly depress the LH activity in ovariectomized rat plasma. Pretreatment of these ovariectomized rats with estradiol benzoate rendered them more sensitive to the effects of progesterone in that 4 mg progesterone/day was then able to significantly depress the LH activity in their plasma. It was concluded that progesterone alone has a feeble inhibitory effect on the secretion of LH but that estrogen pretreatment sensitizes the animal to this inhibitory action of progesterone.

Modulation of pituitary responsiveness to LHRH by androgens in ovariectomized female rats

1977 ◽  
Vol 55 (2) ◽  
pp. 188-192
Author(s):  
Padmaja N. Kulkarni ◽  
Alan A. Simpson ◽  
William H. Moger
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Releasing Hormone ◽  
Daily Dose ◽  
17Β Estradiol ◽  
High Doses ◽  
Pronounced Inhibition

The effect of androgens on pituitary response to luteinizing-hormone-releasing hormone (LHRH) and their ability to modify effects of 17β-estradiol (E2) on pituitary responsiveness to LHRH were tested in ovariectomized rats maintained on a daily dose of 0.25 μg estradiol benzoate per rat for 6 d before androgen administration.Testosterone propionate (TP) (4, 40, 400, or 4000 μg per rat), administered 24 h before LHRH (500 ng per rat), had no significant effect on luteinizing hormone (LH) or follicle-stimulating hormone (FSH) response. Similar doses of dihydrotestosterone (DHT) did not significantly alter the LH response but significantly suppressed the FSH response. Even the lowest dose completely blocked the FSH response to LHRH. TP in combination with 4 or 400 μg of E2 suppressed the stimulatory effect of E2 on both LH and FSH response to LHRH in a dose-related manner. DHT and E2 in combination affected LH response inconsistently, whereas their ratio determined FSH response; there was pronounced inhibition of FSH response in rats given high doses of DHT combined with low doses of E2; DHT inhibition of FSH response in animals receiving 4 μg of DHT with 400 μg E2 was partially overcome by the stimulatory effect of E2. Our results indicate that TP and DHT affect LH and FSH response to LHRH differently. The ratio of androgen to estrogen is important in determining the response to LHRH.

Control of follicle-stimulating hormone secretion by steroid-free bovine follicular fluid in the ovariectomized rat

1983 ◽  
Vol 99 (1) ◽  
pp. 1-8 ◽  
Author(s):  
T. R. Koiter ◽  
G. C. J. van der Schaaf-Verdonk ◽  
H. Kuiper ◽  
N. Pols-Valkhof ◽  
G. A. Schuiling
Keyword(s):  
Luteinizing Hormone ◽  
Follicular Fluid ◽  
Hormone Secretion ◽  
Ovariectomized Rats ◽  
Ovariectomized Rat ◽  
Releasing Hormone ◽  
Basal Release ◽  
Lh Release ◽  
Lh Releasing Hormone ◽  
Lh Secretion

The effects of steroid-free bovine follicular fluid (bFF) and sodium phenobarbitone on spontaneous LH releasing hormone (LHRH)-induced secretion of FSH and LH were studied in ovariectomized rats. Luteinizing hormone releasing hormone was administered by infusion to rats anaesthetized with phenobarbitone. Bovine follicular fluid reduced FSH release and synthesis. Luteinizing hormone release remained unaffected after bFF treatment. Phenobarbitone reduced both FSH and LH release. The observed suppressive effects of bFF and phenobarbitone on FSH secretion were additive, suggesting that the basal release of FSH has an LHRH-dependent and an LHRH-independent component. Furthermore, bFF did not affect pituitary responsiveness of LH secretion to LHRH and reduced the responsiveness of FSH secretion only when administered some time before the LHRH challenge. The present observations support the view that in the ovariectomized rat the pituitary gland is the only site of action of inhibin-like activity as present in bFF.

Estradiol increases glucagon's satiating potency in ovariectomized rats

2001 ◽  
Vol 281 (4) ◽  
pp. R1290-R1294 ◽  
Author(s):  
Nori Geary ◽  
Lori Asarian
Keyword(s):  
Signaling Pathway ◽  
Food Access ◽  
Estradiol Benzoate ◽  
Inhibitory Effect ◽  
Sesame Oil ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Hepatic Portal Vein ◽  
Hepatic Portal

Estradiol decreases meal size, food intake, and body weight in female rats. To investigate whether these effects of estradiol involve a change in the sensitivity of the signaling pathway through which pancreatic glucagon released during meals contributes to meal termination (satiation), glucagon or glucagon antibodies were infused via the hepatic portal vein in ovariectomized rats that were chronically treated with estradiol benzoate (2 μg/day sc) or vehicle alone (100 μl sesame oil). Infusions began at 1 h after dark onset, as rats were refed after 7 h of food deprivation. Glucagon (3 μg/min for 30 min) decreased feeding during the initial 45 min of food access in both groups of rats, but the inhibition was significantly greater in estradiol- than in oil-treated rats. Similarly, antagonism of endogenous glucagon by infusion of glucagon antibodies (a dose neutralizing 3 ng of glucagon in vitro during the first 3 min of refeeding) increased feeding significantly more in estradiol- than in oil-treated rats. These data indicate that an increase in the activity of the endogenous glucagon satiation-signaling pathway may be part of the mechanism for estradiol's inhibitory effect on feeding.

Transient reduction in trabecular bone formation after discontinuation of administration of oestradiol-17β to ovariectomized rats

1993 ◽  
Vol 137 (3) ◽  
pp. 497-503 ◽  
Author(s):  
J. H. Tobias ◽  
T. J. Chambers
Keyword(s):  
Bone Formation ◽  
Trabecular Bone ◽  
Marked Decrease ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Oestrogen Treatment ◽  
Early Effect ◽  
Oestrogen Deficiency ◽  
Old Rats ◽  
Stimulation Of

ABSTRACT While the osteopenia associated with oestrogen deficiency is thought to arise from a relative defect in bone formation with respect to resorption, oestrogen administration itself leads to a decrease, rather than an increase, in bone formation. This decrease in bone formation, which arises from oestrogen's inhibitory effect on bone turnover, presumably masks any underlying tendency of oestrogen treatment towards stimulation of bone formation. To investigate this further, we have examined the early effect of discontinuing the administration of oestradiol-17β (OE2; 40 μg/kg on bone formation indices in ovariectomized 13-week-old rats, before the turnover-induced increase in formation occurs. Histomorphometric indices were assessed at the proximal tibial metaphysis 0, 7, 10, 13 and 16 days following discontinuation of OE2 treatment. Measurements of body weight, uterine weight and longitudinal growth rate confirmed that there were rapid effects of OE2 deficiency on these parameters. We could detect no significant increase in bone resorption, as measured by osteoclast surface and number, until 16 days after ending treatment with OE2; this was coincidental with a reduction in bone volume. Shorter periods of OE2 deficiency were associated with a marked decrease in bone formation, as assessed by dynamic histomorphometric indices. This inhibition of bone formation was largely due to a reduction in double fluorochrome-labelled trabecular surfaces, which were decreased by approximately 70%. We conclude that ending OE2 administration in ovariectomized rats caused a striking decrease in trabecular bone formation, if such indices are assessed prior to the subsequent turnover-induced increase in formation. This suggests that oestrogen treatment in ovariectomized rats is associated with a stimulatory effect on bone formation, in addition to its recognized anti-resorptive action. Journal of Endocrinology (1993) 137, 497–503

Estrogen inhibition of LH and FSH secretion: effects of a GnRH antagonist

1986 ◽  
Vol 250 (4) ◽  
pp. E341-E345
Author(s):  
M. C. Charlesworth ◽  
N. B. Schwartz
Keyword(s):  
Luteinizing Hormone ◽  
Negative Feedback ◽  
Gnrh Antagonist ◽  
Follicle Stimulating Hormone ◽  
Estradiol Benzoate ◽  
Gonadotropin Releasing Hormone ◽  
Ovariectomized Rats ◽  
Inhibitory Effects ◽  
Dependent Component ◽  
Lh Secretion

Follicle-stimulating hormone (FSH) levels are not suppressed as rapidly or to the same degree as luteinizing hormone (LH) levels in ovariectomized rats treated with either gonadotropin-releasing hormone (GnRH) antagonist or estrogen. The acute inhibitory effects of various doses of estrogen on FSH and LH secretion were examined in cannulated, 2-wk ovariectomized rats. No dose of 17 beta-estradiol, up to 2,500 ng injected intravenously, suppressed FSH, although LH secretion was inhibited 50% within 1 h by 100 ng. In another experiment, estradiol benzoate (EB; 10 or 250 micrograms; sc injection in oil) was only marginally effective in suppressing FSH, compared with LH, levels in serum. Treatment with EB 24 h before or after a 500 micrograms dose of a GnRH antagonist did not reduce LH or FSH to levels lower than those achieved with antagonist alone. These results indicate that the GnRH-dependent component of FSH release and the GnRH-independent component that is unmasked in the presence of GnRH antagonist are sensitive to negative feedback by estrogen, indicating that this steroid is not the primary inhibitory ovarian factor regulating FSH in the rat.

ÉTUDES IN VIVO SUR LE MÉTABOLISME DES ANDROGÉNES APRES ADMINISTRATION DE STÉROÏDES INHIBITEURS DE L'OVULATION

1965 ◽  
Vol 50 (1) ◽  
pp. 131-144 ◽  
Author(s):  
P. Mauvais-Jarvis ◽  
M. F. Jayle ◽  
J. Decourt ◽  
J. Louchart ◽  
J. Truffert
Keyword(s):  
Luteinizing Hormone ◽  
Urinary Excretion ◽  
Normal Subjects ◽  
Hormone Activity ◽  
Testosterone Production ◽  
Normal Men ◽  
Ethinyl Oestradiol

ABSTRACT Normal subjects and hirsute women with micropolycystic ovaries were treated with ethinyl-oestrenol + 3-methoxy-ethinyl-oestradiol (Lyndiol®), in view of studying the action of this compound on the production of androgens and on the urinary excretion of their metabolites. In normal men, the production of testosterone and the excretion of androsterone and aetiocholanolone are suppressed, whereas the excretion of other 17-ketosteroids and the production of dehydroepiandrosterone sulphate are unchanged. Moreover, the luteinizing hormone activity (LH) in plasma is depressed. It seems that the preparation inhibits specifically the testicular androgen production, by suppressing the hypothalamo-hypophyseal control of LH. Testosterone production and urinary 17-ketosteroid excretion are modified in the same way in women with Stein-Leventhal's syndrome. Physiopathological and therapeutical implications which come from these results are discussed.

POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE
Keyword(s):  
Inhibitory Action ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Immature Rat ◽  
Rat Strain ◽  
Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

HORMONAL REQUIREMENTS FOR THE MAINTENANCE OF OESTRADIOL-INDUCED INHIBITION OF UTERINE SENSITIVITY IN THE OVARIECTOMIZED RAT

1970 ◽  
Vol 46 (3) ◽  
pp. 341-346 ◽  
Author(s):  
K. P. MEYERS
Keyword(s):  
Subcutaneous Injection ◽  
Ovariectomized Rats ◽  
Ovariectomized Rat ◽  
Single Subcutaneous Injection ◽  
The Third ◽  
Oestradiol Treatment ◽  
Progesterone Treatment ◽  
Endometrial Scratching

SUMMARY Ovariectomized rats treated with 2·5 or 5·0 mg. progesterone daily received a single subcutaneous injection of 0·2 μg. oestradiol on the third day of the progesterone treatment. The deciduomal response to trauma by endometrial scratching was used to determine the degree of uterine sensitivity at various times after oestradiol. Uterine sensitivity was partially and then completely lost 36 and 48 hr. after oestradiol administration. The inhibition of uterine sensitivity persisted until 9 and 11 days after oestradiol when the animals received 2·5 and 5·0 mg. progesterone daily. Uterine sensitivity was completely inhibited on day 11 with doses of oestradiol from 0·2 to 0·05 μg. Withdrawal of progesterone treatment for 48 or 72 hr., but not for 24 hr., after oestradiol treatment restored uterine sensitivity. These results show that the oestradiol-induced inhibition of uterine sensitivity in the progestational endometrium is maintained by continuous progesterone treatment and that the duration of this effect is dependent on the dose of progesterone given.

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