Clomiphene citrate induces luteinizing hormone release through hypothalamic luteinizing hormone-releasing hormone in vitro

1983 ◽  
Vol 103 (3) ◽  
pp. 289-292 ◽  
Author(s):  
A. Miyake ◽  
K. Tasaka ◽  
T. Sakumoto ◽  
Y. Kawamura ◽  
Y. Nagahara ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Clomiphene Citrate ◽  
Female Rats ◽  
Normal Female ◽  
Releasing Hormone ◽  
Superfusion System ◽  
In Series ◽  
Lh Release ◽  
Lh Releasing Hormone

Abstract. The releasing effects of clomiphene citrate (clomiphene) on luteinizing hormone (LH) and LH-releasing hormone (LRH) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were superfused in sequence with medium containing 2 × 10−10 m oestradiol (E2), two significant peaks in LH release (60–130% increase, P < 0.05) were observed 40 min and 90 min after the administration of 3 × 10−8 mol clomiphene. Administration of clomiphene in medium without E2 induced a low peak (25–50% increase, P < 0.05) of LH released from the pituitary perfused in series with the MBH. Administration of clomiphene did not cause a marked increase of LH from the pituitary superfused alone, when superfused with or without E2 containing medium. The concentration of LRH in the efflux was significantly increased (50–100%) 40 min and 90 min after clomiphene administration when MBH was superfused with medium containing E2, whereas clomiphene had no effect when superfused with medium alone. These data indicate: 1) that clomiphene induces LRH release from the MBH, that it may induce LH release, in part, by acting directly at the pituitary level; 2) that changes in LH after clomiphene administration coincide with LRH release, and 3) that a certain concentration of E2 may be necessary for the secretion of LRH by clomiphene.

Hydrocortisone elicits the effect of clomiphene citrate on luteinizing hormone-releasing hormone release in vitro

1984 ◽  
Vol 107 (2) ◽  
pp. 145-148 ◽  
Author(s):  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Tetsuro Sakumoto ◽  
Yasuhito Nagahara ◽  
Toshihiro Aono
Keyword(s):  
Luteinizing Hormone ◽  
Clomiphene Citrate ◽  
Female Rats ◽  
Normal Female ◽  
Releasing Hormone ◽  
In Series ◽  
Significant Release ◽  
Lh Release ◽  
Lh Releasing Hormone

Abstract. The effect of hydrocortisone on the release of luteinizing hormone (LH) and LH-releasing hormone (LRH) in response to clomiphene citrate (clomiphene) were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were perifused in sequence with medium containing 5 × 10−6 m hydrocortisone, a significant release in LH (100– 150% increase, P < 0.01–P < 0.05) was observed 40 min after the administration of 3 × 10−8 mol clomiphene. Clomiphene had no effect on LH release from the pituitary when perifused in series with the MBH without basal hydrocortisone infusion. Administration of clomiphene did not cause a significant increase in LH from the pituitary perifused alone, with or without medium containing hydrocortisone. The concentration of LRH in the efflux was significantly increased 40 min after clomiphene administration when MBH was perifused with medium containing hydrocortisone, whereas clomiphene had no effect when perifused with medium only. These data indicate that hydrocortisone stimulates the effect of clomiphene on LRH release from the hypothalamus, which in turn induces LH release from the pituitary.

Prostaglandin D2 induces release of luteinizing hormone from the rat pituitary gland without the modulation of hypothalamic luteinizing hormone releasing hormone

1983 ◽  
Vol 99 (2) ◽  
pp. 289-292 ◽  
Author(s):  
K. Tasaka ◽  
A. Miyake ◽  
T. Sakumoto ◽  
T. Aono ◽  
K. Kurachi
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Direct Action ◽  
Female Rats ◽  
Prostaglandin D2 ◽  
Medial Basal Hypothalamus ◽  
Releasing Hormone ◽  
In Series ◽  
Lh Release ◽  
Lh Releasing Hormone

The effect of prostaglandin D2 (PGD2) on release of LH and LH releasing hormone (LHRH) was studied in a sequential double-chamber superfusion system using the medial basal hypothalamus (MBH) and the pituitary gland from female rats at dioestrus. Infusion of PGD2 (5·7 or 57μmol/l) caused a significant (P <0·05) increase in LH release to values 40–60% above the preinjection values from the pituitary gland superfused either alone or in series with the MBH. No release of LHRH in response to PGD2 was observed from the superfused MBH. These data demonstrate that PGD2 causes LH release from the pituitary gland not by inducing release of hypothalamic LHRH but by a direct action on the gland.

Wen-Jing-Tang, a Traditional Chinese Herbal Medicine Increases Luteinizing Hormone Release In Vitro

1986 ◽  
Vol 14 (03n04) ◽  
pp. 157-160 ◽  
Author(s):  
Akira Miyake ◽  
Jin-Woo Lee ◽  
Keiichi Tasaka ◽  
Shirou Ohtsuka ◽  
Toshihiro Aono
Keyword(s):  
Herbal Medicine ◽  
Luteinizing Hormone ◽  
Chinese Herbal Medicine ◽  
Female Rats ◽  
Normal Female ◽  
Traditional Chinese Herbal Medicine ◽  
Chinese Herbal ◽  
Lh Release ◽  
Lh Rh

For examination of the effect on luteinizing hormone (LH) release of Wen-Jing-Tang, a traditional Chinese herbal medicine, the pituitary from normal female rats in diestrus was perifused alone or in sequence with the mediobasal hypothalamus (MBH) in a sequential double-chamber perifusion system. Wen-Jing-Tang at 5 or 500 μg/ml induced significant LH release (60-95 % increase) from the pituitary in series with the MBH, but had no effect on LH release from the pituitary perifused alone. These data suggest that Wen-Jing-Tang induces LH release from the pituitary through hypothalamic LH-RH.

Estradiol stimulation of LH response to LHRH and LHRH binding in pituitary cultures

1982 ◽  
Vol 242 (6) ◽  
pp. E392-E397
Author(s):  
L. K. Tang ◽  
A. C. Martellock ◽  
J. K. Horiuchi
Keyword(s):  
Cell Proliferation ◽  
Luteinizing Hormone ◽  
Priming Effect ◽  
Cultured Cells ◽  
Female Rats ◽  
Releasing Hormone ◽  
Lh Release ◽  
Estradiol Stimulation ◽  
Lh Releasing Hormone ◽  
Stimulation Of

The relationship between 17 beta-estradiol (E2) stimulation of luteinizing hormone (LH) response to LH-releasing hormone (LHRH) and E2 effect on LHRH binding was examined in pituitary monolayer cultures prepared from female rats. E2 pretreatment significantly (P less than 0.05) augmented the LHRH-induced LH release to 158-180% of the non-E2-treated controls. The maximal E2-priming effect could be observed after 1 day of treatment. E2 treatment for 3 days stimulated [D-Ala6]luteinizing hormone-releasing hormone (LHRHa) binding to about 1.5-fold that of the non-E2-treated controls without affecting the dissociation constant of LHRH receptor (Kd = 4 X 10(-10) M). The stimulatory effect of E2 on cell proliferation as determined by [3H]thymidine incorporation was also observed 3 days after treatment. However, E2 stimulation of LH accumulation in the cultured cells could be detected as early as 4 h after treatment. These results indicate that E2-priming effect on pituitary LH response to LHRH is initially associated with an increase in cellular LH content and later associated with increases in LHRH binding and in an index of cell proliferation that may include the LH-producing cells.

Vasoactive intestinal peptide stimulates gonadotropin-releasing hormone release from rat hypothalamus in vitro

1988 ◽  
Vol 117 (3) ◽  
pp. 399-402 ◽  
Author(s):  
Shirou Ohtsuka ◽  
Akira Miyake ◽  
Takamichi Nishizaki ◽  
Keiichi Tasaka ◽  
Osamu Tanizawa
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Normal Female ◽  
Gnrh Release ◽  
In Series ◽  
Significant Release ◽  
Lh Release ◽  
Perifusion System

Abstract. The effects of vasoactive intestinal peptide (VIP) on the releases of LH and GnRH were examined in a sequential double chamber perifusion system by perifusing the medio-basal hypothalamus and/or pituitary excised from normal female rats in diestrus or ovariectomized rats. When the medio-basal hypothalamus and pituitary from normal rats in series were perifused with VIP (10−6 mol/l), the concentration of LH in the efflux was increased by 59–181% above that before the injection (P < 0.05), VIP having a dosedependent effect. VIP had no effect on LH release from the pituitary perifused alone. Infusion of VIP at 10−6 mol/l induced a significant release (84–159% increase, P < 0.05) of GnRH from the medio-basal hypothalamus. Infusion of 10−6 mol/l VIP induced a significant release (41–99% increase, P < 0.05) of LH in ovariectomized rats. These findings suggest that VIP induces GnRH release from the medio-basal hypothalamus, resulting in LH release from the pituitary, and that this process does not require ovarian estrogen.

Effects of chronic treatment with oestrogen, an oestrogen antagonist and a potent luteinizing hormone releasing hormone agonist analogue on pituitary responsiveness to luteinizing hormone releasing hormone in the rat

1983 ◽  
Vol 98 (3) ◽  
pp. 313-321 ◽  
Author(s):  
J. M. Hall ◽  
S. A. Whitehead
Keyword(s):  
Luteinizing Hormone ◽  
Chronic Treatment ◽  
Ex Vivo ◽  
Significant Rise ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Serum Lh ◽  
Lh Release ◽  
Lh Releasing Hormone

The rise in gonadotrophin release which occurs after ovariectomy is caused by steroid withdrawal resulting in an enhanced pituitary responsiveness to LH releasing hormone (LHRH) associated with increased LHRH release and pituitary LHRH binding. The effects of oestrogen replacement after ovariectomy and chronic treatment of intact rats with an oestrogen antagonist, tamoxifen, on LH release and in-vitro pituitary responses to LHRH have been investigated. Capsules containing crystalline oestradiol, implanted at the time of ovariectomy, completely inhibited the rise in LH release although pituitary responsiveness was greater after 10 days in the oestrogen-treated rats than in untreated ovariectomized controls. On day 4 after ovariectomy pituitary responses to LHRH were comparable in both treated and untreated groups although in both groups the responses were greater than those measured in intact dioestrous rats. Treatment with tamoxifen over a 4-day period also augmented pituitary responsiveness but only at the lowest dose (0·5 mg/kg); no effect on serum LH concentrations was observed. Higher doses of the antagonist (1 and 2 mg/kg) did not affect pituitary responses, although the highest dose did cause a significant rise in serum LH. Treatment with a daily dose of 50 ng [d-Ser(But)6]LHRH(1–9)nonapeptide-ethylamide, starting on the day of ovariectomy, markedly attenuated the LH responses to LHRH ex vivo at days 2, 4 and 10 after ovariectomy. In contrast, the analogue treatment did not abolish the rise in LH release but this was proportionately less than in controls.

Epidermal growth factor stimulates secretion of rat pituitary luteinizing hormone in vitro

1985 ◽  
Vol 108 (2) ◽  
pp. 175-178 ◽  
Author(s):  
Akira Miyake ◽  
Keiichi Tasaka ◽  
Shirou Otsuka ◽  
Hiroko Kohmura ◽  
Hiroshi Wakimoto ◽  
...  
Keyword(s):  
Growth Factor ◽  
Luteinizing Hormone ◽  
Epidermal Growth Factor ◽  
Female Rats ◽  
Gonadotrophin Secretion ◽  
Significant Release ◽  
Lh Release ◽  
Epidermal Growth ◽  
Lh Releasing Hormone

Abstract. The effects of epidermal growth factor (EGF) on pituitary luteinizing hormone (LH) release and on the releases induced by oestradiol (E2) and LH-releasing hormone (LRH) were examined in a sequential double chamber perifusion system. In this system the mediobasal hypothalami (MBH) and/or pituitaries excised from normally cycling female rats in dioestrus were perifused with test media. Perifusion with EGF at 1 ng/ml for 30 min induced significant release (80–100% increase, P <0.05) of LH from hypothalamo-pituitary pairs, but not from the pituitary alone. Perifusion of the pituitary alone with medium containing 1 ng/ml EGF, resulted in significant release of LH (70–140% increase, P < 0.05) after adminnistration of 10−7 m E2, but did not significantly influence LH release in response to 20 ng/ml LRH. These findings suggest that EGF may be involved in the regulation of pituitary gonadotrophin secretion by a direct effect on the hypothalamus and indirectly by increasing the pituitary responsiveness to E2.

DEPENDENCE ON PROTEIN SYNTHESIS OF THE N6-MONOBUTYRYL CYCLIC AMP PLUS THEOPHYLLINE MEDIATED RELEASE OF LUTEINIZING HORMONE INDUCED BY LUTEINIZING HORMONE RELEASING HORMONE FROM RAT PITUITARY GLANDS IN VITRO

1981 ◽  
Vol 88 (3) ◽  
pp. 329-338 ◽  
Author(s):  
J. DE KONING ◽  
J. A. M. J. VAN DIETEN ◽  
A. M. I. TIJSSEN ◽  
G. P. VAN REES
Keyword(s):  
Protein Synthesis ◽  
Luteinizing Hormone ◽  
Cyclic Amp ◽  
Female Rats ◽  
Releasing Hormone ◽  
Pituitary Tissue ◽  
Pituitary Glands ◽  
Lh Release ◽  
Lh Rh ◽  
Lh Releasing Hormone

The involvement of cyclic AMP in the action of LH releasing hormone (LH-RH) on LH secretion was studied by incubating pituitary glands from adult female rats on day 2 of dioestrus with 1 mm-N6-monobutyryl cyclic AMP (mbcAMP) and 10 mm-theophylline for periods of up to 10 h. This treatment induced a pattern of LH release similar to that observed in the presence of a low concentration of LH-RH (0·1 ng LH-RH/ml), i.e. an initial 4 h period during which the release of LH was minimal was followed subsequently by an increased rate of release. In this system inhibition of protein synthesis by cycloheximide (25 μg/ml) did not impair the initial response of the pituitary tissue but the increase in the rate of LH release during the second phase of the response was blocked. Preincubation with mbcAMP and theophylline increased the responsiveness of the pituitary tissue to LH-RH. This action could be prevented by including cycloheximide during the preincubation period, whereas addition of this drug during the incubation with LH-RH no longer impaired the increased responsiveness. The size of the sensitizing action of mbcAMP and theophylline mediated through the induction of protein synthesis was comparable with that of a high concentration of LH-RH. From the absence of a significant change in total LH during the preincubation period, it was concluded that the increased responsiveness was not the result of newly synthesized LH. The present results suggest a role or roles for cyclic AMP in the secretion of LH induced by LH-RH. Besides an effect on the formation of a factor related to the synthesis of protein, other than LH which has a permissive role in the acute release of LH, cyclic AMP might also be concerned in the secretion process through a pathway which does not involve synthesis of protein.

Substance P stimulates gonadotropin-releasing hormone release from rat hypothalamus in vitro with involvement of oestrogen

1987 ◽  
Vol 115 (2) ◽  
pp. 247-252 ◽  
Author(s):  
Shirou Ohtsuka ◽  
Akira Miyake ◽  
Takamichi Nishizaki ◽  
Keiichi Tasaka ◽  
Toshihiro Aono ◽  
...  
Keyword(s):  
Substance P ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Normal Female ◽  
Dependent Manner ◽  
Gnrh Release ◽  
In Series ◽  
Significant Release ◽  
Lh Release

Abstract. The effects of substance P on the release of LH and GnRH were examined in a sequential double-chamber perifusion system by perifusing the medio-basal hypothalamus and/or pituitary excised from normal female rats in dioestrus or ovariectomized rats. When the medio-basal hypothalamus and pituitary from normal rats were perifused in series with substance P (10−6 mol/l), the concentration of LH in the efflux was significantly (P < 0.05) increased by 70– 120% compared with that before the injection, but substance P had no effect on LH release from the pituitary perifused alone. This LH release by substance P increased in a dose-dependent manner and was blocked by substance P antagonist. Administration of 10−6 mol/l substance P induced a significant release (40–80% increase, P < 0.05) of GnRH from the medio-basal hypothalamus. Infusion of 10−6 mol/l substance P induced significant release (50–100% increase, P < 0.05) of LH and GnRH in ovariectomized rats with an implanted oestradiol capsule, but caused no significant increase in LH release in ovariectomized rats without an oestradiol capsule. Progesterone injection to both ovariectomized rats and ovariectomized rats with an implanted oestradiol capsule had no significant effect on the response of LH to substance P. These findings suggest that substance P induces GnRH release from the medio-basal hypothalamus, resulting in LH release from the pituitary, and that oestrogen may be involved in these processes.

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