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.

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.

Effects of LHRH and ANG II on prolactin stimulation are mediated by hypophysial AT1 receptor subtype

1994 ◽  
Vol 266 (2) ◽  
pp. E274-E278 ◽  
Author(s):  
D. Becu-Villalobos ◽  
I. M. Lacau-Mengido ◽  
S. M. Thyssen ◽  
G. S. Diaz-Torga ◽  
C. Libertun
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Receptor Subtype ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Prolactin Release ◽  
Luteinizing Hormone Releasing Hormone ◽  
Prolactin Response

We have used the nonpeptide angiotensin II (ANG II) receptor antagonists losartan (receptor subtype AT1) and PD-123319 (AT2) to determine the participation of ANG II receptor subtypes in luteinizing hormone-releasing hormone (LHRH)-induced prolactin release in a perifusion study using intact pituitaries in vitro. LHRH (1.85 x 10(-7) M) released prolactin consistently, whereas losartan (10(-5) M) abolished prolactin response without modifying basal prolactin or luteinizing hormone (LH) and follicle-stimulating hormone (FSH) release. PD-123319 (10(-5) M) had no effect on basal or LHRH-induced prolactin, LH, or FSH release. We also determined that the effect of ANG II on prolactin release was mediated by the same receptor subtype. In adenohypophysial cells dispersed in vitro ANG II (10(-8) M) released prolactin. Losartan (10(-7) and 10(-6) M), but not PD-123319, inhibited this effect. We conclude that in intact hypophyses of 15-day-old female rats the effect of LHRH on prolactin release is readily demonstrated. LHRH-induced prolactin release appears to be mediated by ANG II acting in a paracrine manner on AT1 receptors located on lactotrophs.

STEROID PRIMING OF THE LUTEINIZING HORMONE RESPONSE TO LUTEINIZING HORMONE RELEASING HORMONE

1978 ◽  
Vol 77 (3) ◽  
pp. 293-299 ◽  
Author(s):  
L. V. BECK ◽  
M. BAY ◽  
A. F. SMITH ◽  
D. KING ◽  
R. LONG
Keyword(s):  
Luteinizing Hormone ◽  
Female Rats ◽  
Male Rats ◽  
Ovariectomized Rats ◽  
Normal Male ◽  
Initial Exposure ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Lh Rh

Perifusion experiments were performed to study the stimulatory effects of luteinizing hormone releasing hormone (LH-RH) on the release of LH from anterior pituitary tissue. Exposure of pituitary tissue from normal male rats to LH-RH (5 ng/ml for 5 min) induced a small release of LH; in tissue from ovariectomized rats receiving no pretreatment, the release was more than three times greater and in tissue from gonadectomized male or female rats pretreated with oestradiol benzoate and progesterone, the release was six times greater than that observed in normal rats. Further exposure of pituitary tissue from gonadectomized steroid-pretreated male and female rats to LH-RH (5 ng/ml) induced an increase in the level of LH even greater than that seen after the initial exposure (priming action of LH-RH); in tissue from ovariectomized rats receiving no pretreatment, less LH was released than after the first exposure to LH-RH and in tissue from normal male rats the response was unchanged.

scholarly journals Effect of leptin on LH and FSH release in ovariectomized rats

2002 ◽  
Vol 08 (01) ◽  
pp. 105-113
Author(s):  
M. M. Shebl
Keyword(s):  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Significant Recovery ◽  
Hormonal Release ◽  
Stimulating Hormone

We compared the estradiol/progesterone-induced luteinizing hormone [LH] and follicle-stimulating hormone [FSH] release between normally fed and leptin-supplemented starved ovariectomized female rats and studied also the effect of hyper-leptinaemia on the steroid-induced hormonal release in normally fed ovariectomized rats. Three days’ starvation completely abolished steroid-induced LH and FSH release. Significant recovery of the hormonal release was shown in the leptin-supplemented starved group. The magnitudes of LH and FSH release in the normally fed animals with a higher dose of leptin were statistically the same as those in the normally fed group without leptin. These observations indicate that physiological concentrations of circulating leptin exert a stimulatory effect on steroid-induced LH and FSH release.

Effect of Starvation on Pituitary and Serum Follicle-Stimulating Hormone and Luteinizing Hormone Following Ovariectomy in the Rat

1972 ◽  
Vol 50 (8) ◽  
pp. 768-773 ◽  
Author(s):  
E. A. Ibrahim ◽  
B. E. Howland
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Follicle Stimulating Hormone ◽  
Female Rats ◽  
Intact Female ◽  
Pituitary Glands ◽  
Ad Libitum ◽  
Stimulating Hormone

The concentration of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in serum and pituitary glands was studied in intact female rats and rats that were ovariectomized on day 0 of the experiment and then starved or fed for 2, 4, 7, or 9 days. Ovariectomy resulted in enhanced rates of synthesis and release of FSH and LH as indicated by the significant (P < 0.01) rises in the concentration of both hormones in the pituitary gland and serum.Starvation resulted in a decrease in body and pituitary weight. The concentration of FSH and LH in pituitary glands of starved rats was higher (P < 0.05) than that in fed rats on days 7 and 9. The concentration of FSH and LH in serum of starved rats was increased after ovariectomy but the levels on days 7 and 9 were lower than those of fed rats.These results suggest that the synthesis of FSH and LH was enhanced in both starved and fed rats following ovariectomy while the rate of release of both hormones was decreased at 7 and 9 days of starvation in comparison with rats fed ad libitum.

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