SUPPRESSION OF THE LUTEINIZING HORMONE RELEASING EFFECT OF LUTEINIZING HORMONE RELEASING HORMONE BY ARGININE-VASOTOCIN

1979 ◽  
Vol 81 (1) ◽  
pp. 103-108 ◽  
Author(s):  
K. YAMASHITA ◽  
M. MIENO ◽  
ER. YAMASHITA
Keyword(s):  
Luteinizing Hormone ◽  
Carotid Artery ◽  
Pituitary Gland ◽  
Standard Dose ◽  
Venous Blood ◽  
Arginine Vasotocin ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Releasing Effect ◽  
Lh Rh

The concentrations of 17-oxosteroids in the spermatic venous blood of anaesthetized dogs were used as an index of LH release to assess the effects of arginine-vasotocin on the response of the canine pituitary gland to exogenous luteinizing hormone releasing hormone (LH-RH). When injected into the carotid artery, arginine-vasotocin (1·0 μg/kg body wt) caused no significant alterations in the testicular output of 17-oxosteroids. The administration of LH-RH (5 μg/kg body wt, a standard dose) into the carotid artery produced typical stimulation of testicular 17-oxosteroid secretion. Administration of arginine-vasotocin (0·01, 0·1 or 1·0 μg/kg body wt) into the carotid artery 3 h before the administration of a standard dose of LH-RH inhibited the testicular secretion of 17-oxosteroids normally induced by LH-RH. However, pretreatment with arginine-vasotocin (1·0 μg/kg body wt) did not affect the testicular response to i.v. administration of human chorionic gonadotrophin (5 i.u./kg body wt). These results indicate that in the dog, arginine-vasotocin inhibits the LH-RH-induced release of LH by acting directly on the anterior pituitary gland.

SUPPRESSION OF THE LUTEINIZING HORMONE RELEASING EFFECT OF LUTEINIZING HORMONE RELEASING HORMONE BY ARGININE-VASOTOCIN IN IMMATURE MALE DOGS

1980 ◽  
Vol 84 (3) ◽  
pp. 449-452 ◽  
Author(s):  
K. YAMASHITA ◽  
M. MIENO ◽  
ER. YAMASHITA
Keyword(s):  
Luteinizing Hormone ◽  
Carotid Artery ◽  
Standard Dose ◽  
Isotonic Saline ◽  
Arginine Vasotocin ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Immature Male ◽  
Lh Rh

Arginine-vasotocin (0·1 or 10 ng/kg body wt) was administered into the carotid artery of anaesthetized immature male dogs 3 h before the administration of a standard dose of luteinizing hormone releasing hormone (LH-RH, 5 μg/kg body wt) into the same vessel. The rate of secretion of 17-oxosteroids by the testes in vivo served as an index of luteinizing hormone (LH) secretion. The administration of LH-RH into the carotid artery of control dogs which had been injected with isotonic saline caused a slight but definite increase in the secretion of testicular 17-oxosteroids. This effect of LH-RH on the testicular secretion of steroids was markedly reduced by pretreatment with arginine-vasotocin. However, the testicular response to the i.v. administration of human chorionic gonadotrophin (5 i.u./kg body wt) was unaffected by pretreatment with arginine-vasotocin (10 ng/kg body wt). These results indicate that in immature male dogs, arginine-vasotocin is able to inhibit the action of LH-RH by acting directly on the anterior pituitary gland.

INHIBITION BY MELATONIN OF THE PITUITARY RESPONSE TO LUTEINIZING HORMONE RELEASING HORMONE IN VIVO

1978 ◽  
Vol 76 (3) ◽  
pp. 487-491 ◽  
Author(s):  
K. YAMASHITA ◽  
M. MIENO ◽  
T. SHIMIZU ◽  
ER. YAMASHITA
Keyword(s):  
Luteinizing Hormone ◽  
Carotid Artery ◽  
Anterior Pituitary ◽  
Chorionic Gonadotrophin ◽  
Human Chorionic Gonadotrophin ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Secretion

The rate of secretion of 17-oxosteroids by the testes of anaesthetized dogs in vivo was used as an index of LH secretion. Intracarotid injection of luteinizing hormone releasing hormone (LH-RH, 1, 5 or 10 μg/kg body wt) resulted in an increase in the testicular 17-oxosteroid secretion which was roughly proportional to the dose administered and which reached a maximum 60 min after the injection. Testicular output of 17-oxosteroids was unaffected by administration of melatonin (10 or 100 μg/kg body wt) into the carotid artery. When LH-RH (5 μg/kg) was injected into the carotid artery 3 h after intracarotid injection of melatonin (10 or 100 μg/kg), the testicular response to LH-RH was considerably diminished. Pretreatment with melatonin (100 μg/kg) did not alter the testicular response to human chorionic gonadotrophin (20 i.u./kg body wt) given i.v. It is concluded that melatonin may act directly on the anterior pituitary gland in dogs to inhibit the LH-RH-induced release of LH.

EFFECT OF SYNTHETIC LUTEINIZING HORMONE RELEASING HORMONE ON OVULATION DURING THE OESTROUS CYCLE IN THE RAT

1974 ◽  
Vol 76 (3) ◽  
pp. 431-437 ◽  
Author(s):  
H. Morishita ◽  
H. Mitani ◽  
Y. Masuda ◽  
K. Higuchi ◽  
M. Tomioka ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Critical Period ◽  
Early Period ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Average Volume ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

ABSTRACT The effect of synthetic luteinizing hormone releasing hormone (LH-RH) on ovulation has been studied during the oestrous cycle in adult female rats. Ovulation could be induced by the administration of 1 μg synthetic LH-RH at 1:00 a. m. on the day of dioestrus II (lights on from 10:00 p.m. to 10:00 a.m.). At 1:00 a.m. on the day of dioestrus II, the average volume of the largest follicles reached a volume of 83 × 106 μm3 and was three fifth of the volume of that at 6:00 a. m. on the day of pro-oestrus (critical period). These findings suggest that the luteinizing hormone (LH) content in the pituitary gland during the early period of dioestrus II is sufficient to induce ovulation and that the follicles that reach to three fifth of the volume at the critical period are capable of ovulating providing endogenous ovulatory LH released.

STUDIES WITH FRAGMENTS OF A HIGHLY ACTIVE ANALOGUE OF LUTEINIZING HORMONE RELEASING HORMONE

1979 ◽  
Vol 81 (2) ◽  
pp. 175-182 ◽  
Author(s):  
J. SANDOW ◽  
W. KÖNIG
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Enzyme Stability ◽  
Organ Distribution ◽  
Structural Requirements ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Highly Active ◽  
Lh Rh

The minimal structural requirements for gonadotrophin releasing activity were studied with fragments of a highly active analogue of luteinizing hormone releasing hormone (LH-RH), [d-Ser(But)6]LH-RH(1–9)nonapeptide-ethylamide (Hoe 766). All fragments are related to the C-terminal structure of LH-RH and have increased enzyme stability. Ovulation in phenobarbitone-blocked rats was induced with a median effective dose/rat, of 1·9 μg of the (3–9)-heptapeptide, Trp-Ser-Tyr-d-Ser(But)-Leu-Arg-Pro-ethylamide and 6·8, 18·0 and 38·3 μg for the (4–9), (5–9) and (6–9) fragments respectively. The (3–9)-heptapeptide and (4–9)-hexapeptide induced release of LH and FSH in phenobarbitone-blocked rats with a ratio similar to that of LH-RH. Degradation of LH-RH by enzyme preparations of liver, kidney and hypothalamic or anterior pituitary tissue was not modified by addition of the (3–9)-heptapeptide fragment. The organ distribution of the 125I-labelled (3–9)-heptapeptide fragments was similar to LH-RH, but not to Hoe 766. The peptide accumulated in liver and kidney, but was eliminated from the anterior pituitary gland 15 min after i.v. injection, whereas Hoe 766 showed progressive accumulation in the pituitary gland (tissue: plasma ratio = 6·6 after 60 min). In contrast to C-terminal fragments of LH-RH, the corresponding fragments of nonapeptide analogues retained significant biological activity, and the minimal structural requirements for LH release may be related to the C-terminal sequence of LH-RH.

SECRETION OF LUTEINIZING HORMONE CAUSED BY CONTINUOUS INFUSIONS OF LUTEINIZING HORMONE RELEASING HORMONE IN THE LONG-TERM OVARIECTOMIZED RAT: EFFECT OF OESTROGEN PRETREATMENT

1976 ◽  
Vol 71 (1) ◽  
pp. 1-11 ◽  
Author(s):  
G. A. SCHUILING ◽  
H. P. GNODDE
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Ovariectomized Rats ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Clear Cut ◽  
Oestradiol Benzoate ◽  
Maximal Plasma ◽  
Lh Rh

SUMMARY Continuous infusions of luteinizing hormone releasing hormone (LH-RH) into phenobarbitone-treated long-term ovariectomized rats, resulted in patterns of LH secretion which were determined by the blood LH-RH concentration. Infusions of 52 ng LH-RH/h caused steadily increasing plasma LH levels, which stabilized after about 2 h of infusion and were maintained for the rest of the experiment (9 h). A similar course of plasma LH concentration was observed as a result of infusions of 104 ng LH-RH/h, though in this case LH concentrations reached higher levels than those induced by infusion of 52 ng LH-RH/h. Higher rates of LH-RH infusion (208 and 416 ng/h), however, induced clear-cut LH peaks, which reached their maximal plasma values after 2–3 h of infusion and then declined again until, at the end of the experiment, they were only slightly higher than the LH levels induced by infusions of 52 ng LH-RH/h. A similar series of LH-RH infusions given to ovariectomized rats pretreated with oestradiol benzoate during 3 days (the rats were injected daily with 7 μg steroid), produced a highly augmented response of the pituitary gland, but all LH-RH concentrations infused induced rather sharp LH peaks, reaching their maximum after 2–3 h of infusion. After 5 h of infusion the descending parts of all these peaks appeared to converge. In both control and oestradiol benzoate-pretreated rats there appeared to be a linear relationship between the logarithm of the blood LH-RH concentration and the maximal plasma LH values on one hand, and the amount of LH secreted during the first 5 h of infusion on the other. Furthermore, it appeared that the longer the period of oestrogen action, the more the response of the pituitary gland to a certain dose of LH-RH was enhanced.

OESTROGEN-INDUCED CHANGES IN THE SECRETION OF LUTEINIZING HORMONE CAUSED BY CONTINUOUS INFUSIONS OF LUTEINIZING HORMONE RELEASING HORMONE IN THE LONG-TERM OVARIECTOMIZED RAT

1977 ◽  
Vol 72 (2) ◽  
pp. 121-126 ◽  
Author(s):  
G. A. SCHUILING ◽  
H. P. GNODDE
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Hormone Secretion ◽  
Potential Response ◽  
Luteinizing Hormone Secretion ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Induced Changes

SUMMARY Oestrogen-induced changes in luteinizing hormone secretion, caused by continuous infusions of luteinizing hormone releasing hormone (LH-RH), appear to depend on the duration of exposure of the pituitary gland to the releasing hormone. The initial oestrogen-induced depression of the potential response of the pituitary gland to LH-RH, which always seems to occur, does not necessarily turn into an enhancement of this potential response. It is suggested that this may be due to the fact that the response of the pituitary gland to LH-RH infusions is a continuously changing parameter influenced by oestrogen.

Priming effect of luteinizing hormone releasing hormone in the hypogonadal mouse

1982 ◽  
Vol 94 (2) ◽  
pp. 283-287 ◽  
Author(s):  
G. Fink ◽  
W. J. Sheward ◽  
H. M. Charlton
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Priming Effect ◽  
Plasma Concentrations ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh ◽  
Lh Releasing Hormone

We have investigated the LH response to LH releasing hormone (LH-RH) in female hypogonadal (hpg) mice in which the hypothalamus contains no LH-RH and the pituitary gland contains significantly less LH than in normal mice. Both the releasing action and the priming effect of LH-RH were not significantly different in hpg compared with normal mice. Raised plasma concentrations of oestradiol-17β reduced pituitary responsiveness to LH-RH in normal but not in hpg mice. These results show that in the mouse neither longterm exposure to normal levels of LH-RH nor a normal pituitary content of LH are necessary for either the releasing or the priming action of LH-RH.

Sign in / Sign up

Export Citation Format

Share Document