Effects of estrogen and progesterone on pulsatile discharges of luteinizing hormone in the ovariectomized rat

1977 ◽  
Vol 55 (2) ◽  
pp. 226-233 ◽  
Author(s):  
Richard F. Weick
Keyword(s):  
Luteinizing Hormone ◽  
Intravenous Injection ◽  
Subcutaneous Injection ◽  
Ovariectomized Rats ◽  
Feedback Signal ◽  
Complete Suppression ◽  
Subcutaneous Implantation ◽  
Apparent Effect ◽  
Effective Feedback ◽  
17Β Estradiol

The effects of both acute and chronic systemic administration of estrogen and progesterone on pulsatile discharges of luteinizing hormone were observed in ovariectomized rats. Intravenous injection of 10 μg of 17β-estradiol resulted in a gradual decrease in plasma luteinizing hormone (LH) concentrations but did not completely block the pulsatile discharges. Subcutaneous implantation of Silastic capsules containing 17β-estradiol caused similar decreases; plasma LH concentrations decreased for the first 6 h but periodic increases continued, with nearly complete suppression of such pulsatile discharges by 24 h. Such inhibition was maintained for the 14-day course of the experiments. Progesterone alone, whether administered by Silastic capsule or by daily subcutaneous injection in oil, was without apparent effect on either plasma LH concentrations or temporal patterns of the hormone. Further, progesterone combined with 17β-estradiol was little, if any, more effective in this regard than estradiol alone. These results indicate that estrogen is an effective feedback signal inhibiting pulsatile release of LH in the rat and that progesterone alone has little, if any, influence in this regard.

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.

Desensitization of the pituitary gland induced in vivo by luteinizing hormone-releasing hormone (LRH) or by the LRH-analogue buserelin does not affect the autonomous secretion of luteinizing hormone and follicle stimulating hormone as observed in vitro

1984 ◽  
Vol 106 (4) ◽  
pp. 454-458 ◽  
Author(s):  
G. A. Schuiling ◽  
H. Moes ◽  
T. R. Koiter
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Normal Level ◽  
Ovariectomized Rats ◽  
Complete Suppression ◽  
Pituitary Glands ◽  
Pre Treatment ◽  
Lh Secretion

Abstract. Three-weeks ovariectomized rats were sc implanted with Alzet® osmotic minipumps which released either LRH or the LRH-analogue buserelin at the rate of 250 ng/h. Control rats were implanted with a silastic 'shampump'. After explantation, 6 days later, the pituitary glands of part of these rats were exposed to the maximally active LRH concentration of 1 μg/ml for a period of 6 h. using a perifusion system. In a second group of rats explantation and perifusion was done not directly, but 5 days after cessation of the I.RH pretreatment. After 6 days in vivo pre-treatment with LRH or with buserelin the pituitary LH and FSH stores were partially depleted, the depletion after buserelin being stronger than after LRH. The pituitary glands of the first group of rats showed rates of both maximally LRH-stimulated and unstimulated (autonomous) LH- and FSH-secretion which were strongly impaired, the impairment after buserelin being stronger than after LRH. In the group with a 5 days interval between in vivo LRH/buserelin pre-treatment and explantation the pituitary LH and FSH stores were restored to the range of pre-treatment levels. Of these pituitaries the autonomous secretion of LH and FSH as well as the maximally LRH-stimulated secretion of FSH was restored to the normal level; the maximally LRH-stimulated secretion of LH, however, remained depressed, indicating that 5 days after cessation of exposure to LRH or to buserelin, and in spite of restored pituitary LH/FSH contents, the sensitivity of the LH releasing system to LRH was still subnormal. The results suggest that the autonomous secretion of LH and FSH as well as the LRH-stimulated secretion of FSH, but not the LRH-stimulated secretion of LH may be dependent on the content of the pituitary LH and FSH stores. Furthermore, after treatment with LRH or buserelin the autonomous secretion of LH may return to a normal level when the sensitivity of the LH releasing system to LRH is still impaired: apparently, the mechanisms underlying the autonomous and the LRH-stimulated LH secretion do not influence each other. It is discussed that in situations in which a complete suppression of the pituitary-gonadal axis is demanded (carcinomata of the breast or the prostate; precocious puberty) desensitization of the pituitary gland with super-active LRH-analogues like buserelin alone is not sufficient, as this does not affect the autonomous secretion of LH and FSH. For total suppression of gonadal activity the pituitary gland must be completely depleted with relatively large doses of analogue.

scholarly journals Less Carcinogenic Chlorinated Estrogens Applicable to Hormone Replacement Therapy

2021 ◽  
Vol 22 (13) ◽  
pp. 7222
Author(s):  
Yoshinori Okamoto ◽  
Hideto Jinno ◽  
Shinji Itoh ◽  
Shinya Shibutani
Keyword(s):  
Hormone Replacement Therapy ◽  
Replacement Therapy ◽  
Hormone Replacement ◽  
Metabolic Activation ◽  
Ovariectomized Rats ◽  
Estrogenic Potential ◽  
Carcinogenic Potential ◽  
Induced Tumors ◽  
Carcinogenic Effects ◽  
17Β Estradiol

Human estrogens prescribed for hormone replacement therapy (HRT) are known to be potent carcinogens. To find safer estrogens, several chlorinated estrogens were synthesized and their carcinogenic potential were determined. A pellet containing either 2-chloro-17β-estradiol (2-ClE2) or 4-chloro-17β-estradiol (4-ClE2) was implanted subcutaneously for 52 weeks into August Copenhagen Irish (ACI) rats, a preferred animal model for human breast cancer. 17β-Estradiol (E2) frequently induced mammary tumors while both 2-ClE2 and 4-ClE2 did not. Their 17α-ethinyl forms, thought to be orally active estrogens, were also synthesized. Neither 2-chloro-17α-ethinylestradiol (2-ClEE2) nor 4-chloro-17α-ethinylestradiol (4-ClEE2) induced tumors. The less carcinogenic effects were supported by histological examination of mammary glands of ACI rats treated with the chlorinated estrogens. A chlorine atom positioned at the 2- or 4-position of E2 may prevent the metabolic activation, resulting in reducing the carcinogenicity. 2-ClE2 and 4-ClE2 administered subcutaneously and 2-ClEE2 and 4-ClEE2 given orally to ovariectomized rats all showed uterotrophic potency, albeit slightly weaker than that of E2. Our results indicate that less carcinogenic chlorinated estrogens retaining estrogenic potential could be safer alternatives to the carcinogenic estrogens now in use for HRT.

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.

The impact of exogenous estrogens on biochemical markers of endothelial dysfunction in diabetic rats with hypoestrogenia

2017 ◽  
Vol 59 (1) ◽  
pp. 46-52
Author(s):  
Tetiana Kiprich ◽  
Nataliia Gorbenko ◽  
Oleksii Borikov ◽  
Olha Ivanova ◽  
K. V. Taran
Keyword(s):  
Endothelial Dysfunction ◽  
Biochemical Markers ◽  
Diabetic Rats ◽  
Ovariectomized Rats ◽  
Receptor Modulator ◽  
17Β Estradiol ◽  
The Impact ◽  
Gender Specific ◽  
Specific Agent

It was investigated the impact of selective estrogen receptor modulator PE0607 comparing to 17β-estradiol on the biochemical markers of endothelial dysfunction in ovariectomized rats with type 2 diabetes. It was established that injection of PE0607 as well as 17β-estradiol decreases lipid peroxidation first products in serum and increases serum whole antioxidant activity and NO-synthase activity in vessels of experimental rats. These results justify the perspectives of compound PE0607 use as a potential gender-specific agent for prevention and treatment of diabetic cardiovascular disorders in women with hypoestrogenia.

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