EFFECTS OF AN ANTI-OESTROGEN, TAMOXIFEN (ICI 46,474), ON LUTEINIZING HORMONE RELEASE AND OVULATION IN THE HEN

The role of oestradiol in the regulation of LH release in the hen was studied by use of the anti-oestrogen, tamoxifen (ICI 46,474). Intramuscular injection of laying hens with 2 or 4 mg tamoxifen on 2 successive days delayed or prevented the occurrence of the preovulatory release of LH and ovulation expected on day 3. Ovulation could be restored by i.v. injection of 20 pg LH releasing hormone (LH-RH). Tamoxifen at a dose of 1 mg affected neither the timing of the preovulatory release of LH nor ovulation. Treatment with 2 or 4 mg tamoxifen on 2 successive days reduced the effectiveness of an i.m. injection of progesterone to stimulate a release of LH. Injection of 1, 2 or 4 mg tamoxifen on 2 successive days significantly raised basal levels of LH in the blood at 24 h after the last injection. This was associated with an increase in the capacity of the pituitary gland to respond to an injection of synthetic LH-RH by a release of LH. These studies suggest that oestradiol has at least two roles in the regulation of LH release in the hen. First, it maintains a low basal level of LH in the blood by reducing the responsiveness of the pituitary gland to LH-RH. Secondly, oestradiol has a facilitative role in the mechanism by which progesterone stimulates the preovulatory release of LH.

Download Full-text

Role of Ca2+ and Na+ on luteinizing hormone release from the calf pituitary

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1988.255.4.e469 ◽

1988 ◽

Vol 255 (4) ◽

pp. E469-E474

Author(s):

J. P. Kile ◽

M. S. Amoss

Keyword(s):

Luteinizing Hormone ◽

Ionophore A23187 ◽

Channel Blockers ◽

Hormone Release ◽

Primary Cells ◽

Rat Pituitary ◽

Voltage Dependent ◽

Lh Release ◽

Ca2 Channels

It has been proposed that gonadotropin-releasing hormone (GnRH) stimulates Ca2+ entry by activation of voltage-independent, receptor-mediated Ca2+ channels in the rat gonadotroph. Little work has been done on the role of calcium in GnRH-induced luteinizing hormone (LH) release in species other than the rat. Therefore, this study was done to compare the effects of agents that alter Ca2+ or Na+ entry on LH release from calf anterior pituitary primary cells in culture. GnRH (100 ng/ml), Ca2+ ionophore A23187 (2.5 microM), and the depolarizing agent ouabain (0.1-10 microM) all produced significant increases (P less than 0.05) in LH release; these effects were significantly reduced when the cells were preincubated with the organic Ca2+ channel blockers nifedipine (1-10 microM) and verapamil (1-10 microM) and with Co2+ (0.01-1 mM). The effect of ouabain was inhibited by tetrodotoxin (TTX; 1-10 nM) as well as by nifedipine at 0.1-10 microM. In contrast to its effect on rat pituitary LH release, TTX significantly inhibited GnRH-stimulated LH release at 1-100 nM. These results suggest that GnRH-induced LH release may employ Ca2+ as a second messenger in bovine gonadotrophs and support recent speculation that GnRH-induced Ca2+ mobilization may in part be voltage dependent.

Download Full-text

RESTORATION OF OESTROGEN POSITIVE FEEDBACK EFFECT ON LH RELEASE BY BROMOCRIPTINE IN HYPERPROLACTINAEMIC PATIENTS WITH GALACTORRHOEA-AMENORRHOEA

Acta Endocrinologica ◽

10.1530/acta.0.0910591 ◽

1979 ◽

Vol 91 (3) ◽

pp. 591-600 ◽

Cited By ~ 19

Author(s):

Toshihiro Aono ◽

Akira Miyake ◽

Takenori Shioji Motoi Yasuda ◽

Koji Koike ◽

Keiichi Kurachi

Keyword(s):

Luteinizing Hormone ◽

Follicle Stimulating Hormone ◽

Serum Prolactin ◽

Serum Luteinizing Hormone ◽

Serum Lh ◽

Lh Release ◽

The Mean ◽

Lh Rh ◽

Lh Releasing Hormone ◽

Positive Feedback Effect

ABSTRACT Five mg of bromocriptine was administered for 3 weeks to 8 hyperprolactinaemic women with galactorrhoea-amernorrhoea, in whom the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to 100 μg of iv LH-releasing hormone (LH-RH) had been evaluated. Twenty mg of conjugated oestrogen (Premarin®) was injected iv any day between the 10th and 12th day from the initiation of the treatment, and serum LH levels were serially determined for 120 h. Hyperresponse of LH with normal FSH response to LH-RH was observed in most patients. Bromocriptine treatment for 10 to 12 days significantly suppressed mean (± se) serum prolactin (PRL) levels from 65.1 ± 23.0 to 10.4 ± 2.0 ng/ml, while LH (12.6 ± 2.1 to 24.8 ± 5.9 mIU/ml) and oestradiol (40.1 ± 7.6 to 111.4 ± 20.8 pg/ml) levels increased significantly. Patients on bromocriptine treatment showed LH release with a peak at 48 h after the injection of Premarin. The mean per cent increases in LH were significantly higher than those in untreated patients with galactorrhoea-amenorrhoea between 32 and 96 h after the injection. The present results seem to suggest that the restoration of LH-releasing response to oestrogen following suppression of PRL by bromocriptine may play an important role in induction of ovulation in hyperprolactinaemic patients with galactorrhoea-amenorrhoea.

Download Full-text

The Role of Neural Inputs from the Posterior Arcuate Nucleus in Pulsatile Luteinizing Hormone Release in Ovariectomized Rats.

Biology of Reproduction ◽

10.1093/biolreprod/83.s1.575 ◽

2010 ◽

Vol 83 (Suppl_1) ◽

pp. 575-575

Author(s):

Yoshihisa Uenoyama ◽

Saya Watanabe ◽

Kinuyo Iwata ◽

Satoshi Ohkura ◽

Kei-ichiro Maeda ◽

...

Keyword(s):

Luteinizing Hormone ◽

Arcuate Nucleus ◽

Ovariectomized Rats ◽

Hormone Release ◽

Luteinizing Hormone Release

Download Full-text

LUTEINIZING HORMONE RELEASING HORMONE-INDUCED RELEASE OF LUTEINIZING HORMONE FROM PITUITARY EXPLANTS OF COWS KILLED BEFORE OR AFTER OESTRADIOL TREATMENT

Journal of Endocrinology ◽

10.1677/joe.0.0880017 ◽

1981 ◽

Vol 88 (1) ◽

pp. 17-25 ◽

Cited By ~ 9

Author(s):

E. M. CONVEY ◽

J. S. KESNER ◽

V. PADMANABHAN ◽

T. D. CARRUTHERS ◽

T. W. BECK

Keyword(s):

Luteinizing Hormone ◽

Pituitary Gland ◽

Lh Surge ◽

Releasing Hormone ◽

Oestradiol Treatment ◽

Readily Releasable Pool ◽

Serum Lh ◽

Pituitary Glands ◽

Lh Rh ◽

Lh Releasing Hormone

In ovariectomized heifers, oestradiol decreases concentrations of LH in serum for approximately 12 h after which LH is released in a surge comparable in size and duration to the preovulatory surge. Using this model, we measured LH release induced by LH releasing hormone (LH-RH) from pituitary explants taken from ovariectomized heifers before or after an oestradiol-induced LH surge. These changes were related to changes in LH concentrations in serum and pituitary glands and hypothalamic LH-RH content. Twenty Holstein heifers were randomly assigned to one of four treatment groups to be killed 0, 6, 12, or 24 h after the injection of 500 μg oestradiol-17β. Jugular blood was collected at −2, −1 and 0 h then at intervals of 2 h until slaughter. Pituitary glands were collected and ≃2 mm3 explants were exposed to 4 ng LH-RH/ml medium for 30 min (superfusion) or 4 ng LH-RH/ml medium for 2 h in Erlenmeyer flasks. Levels of LH were measured in the medium. Hypothalami, collected at autopsy, were assayed for LH-RH content. To determine pituitary LH content, an additional 15 ovariectomized heifers were killed, five each at 0, 12 and 24 h after the injection of 500 μg oestradiol. In both groups of heifers, oestradiol reduced serum LH concentrations to ≃ 1 ng/ml, a level which persisted for 12 h, when LH was released in a surge. Pituitary sensitivity to LH-RH was increased at 6 and 12 h after the injection of oestradiol, but was markedly decreased at 24 h, i.e. after the LH surge. Despite this twofold increase in capacity of the pituitary gland to release LH in response to LH-RH, pituitary LH content did not change during 12 h after oestradiol treatment. However, LH content decreased after the LH surge and this decrease was associated with a decrease in pituitary responsiveness to LH-RH. Hypothalamic LH-RH content was not altered by these treatments. We have interpreted our results as evidence that oestradiol exerts a positive feedback effect on the pituitary gland of ovariectomized heifers such that pituitary sensitivity to LH-RH is increased twofold by the time the LH surge is initiated. In addition, oestradiol causes a transitory inhibition of LH-RH release as shown by the fact that serum LH concentrations remained low during the interval from injection of oestradiol until the beginning of the LH surge despite the fact that pituitary sensitivity to LH-RH is increased at this time. Depletion of a readily releasable pool of pituitary LH may be the mechanism by which the LH surge is terminated.

Download Full-text