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.

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.

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.

Blockade of LH–RH induced ovulation in immature rats by LH–RH antiserum

1976 ◽  
Vol 54 (3) ◽  
pp. 405-408 ◽  
Author(s):  
M. A. Hirsch ◽  
M. L. Givner
Keyword(s):  
Luteinizing Hormone ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Induced Ovulation ◽  
Modified Method ◽  
Immature Rats ◽  
Biological Potency ◽  
Lh Rh

An in vivo method for the determination of biological potency of luteinizing hormone -releasing hormone (LH–RH) antiserum is described. The procedure involves antiserum blockade of LH–RH induced ovulation in immature rats primed with pregnant mare's serum. A modified method for the induction of LH–RH antibodies in rabbits is also detailed.

INHIBITORY ACTIVITY OF ANALOGUES OF LUTEINIZING HORMONE-RELEASING HORMONE (LH-RH) IN VITRO AND IN VIVO

1976 ◽  
Vol 5 (s1) ◽  
pp. s279-s289 ◽  
Author(s):  
L. FERLAND ◽  
F. LABRIE ◽  
M. SAVARY ◽  
M. BEAULIEU ◽  
D.H. COY ◽  
...  
Keyword(s):  
Luteinizing Hormone ◽  
Inhibitory Activity ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

RELATIVE ACTIVITY, PLASMA ELIMINATION AND TISSUE DEGRADATION OF SYNTHETIC LUTEINIZING HORMONE RELEASING HORMONE AND CERTAIN OF ITS ANALOGUES

1979 ◽  
Vol 80 (1) ◽  
pp. 141-152 ◽  
Author(s):  
A. D. SWIFT ◽  
D. B. CRIGHTON
Keyword(s):  
Luteinizing Hormone ◽  
Pituitary Gland ◽  
Anterior Pituitary ◽  
Inverse Correlation ◽  
Anterior Pituitary Gland ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Lh Rh

The abilities of three nonapeptide analogues of synthetic luteinizing hormone releasing hormone (LH-RH) to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in anoestrous and cyclic ewes were examined, as were their elimination from the plasma in vivo and degradation by extracts of the hypothalamus, anterior pituitary gland, lung, kidney, liver and plasma in vitro. In all cases, comparisons were made with synthetic LH-RH. When injected i.v. into mature ewes as a single dose, the potencies of the analogues were graded and Des Gly-NH210 LH-RH ethylamide was found to be the least potent. It was not possible to demonstrate any significant increase in the potency of this analogue over LH-RH, although a trend was apparent with each parameter examined. [d-Ser(But)6] Des Gly-NH210 LH-RH ethylamide had the greatest potency. There were no differences between the responses of anoestrous ewes and those of ewes treated on day 10 of the oestrous cycle. None of the analogues had a rate of elimination from the plasma different from that of LH-RH during either the first or the second components of the biphasic disappearance curve. The incubation of LH-RH with tissue extracts showed that extracts of the hypothalamus and anterior pituitary gland degraded LH-RH to a similar extent. Both the hypothalamic and anterior pituitary gland extracts degraded more LH-RH than did lung extract, which in turn destroyed more LH-RH than did extracts of kidney or liver tissue. The degradative abilities of kidney and liver extracts did not differ from each other. Plasma failed to degrade LH-RH or the analogues. Although LH-RH was rapidly destroyed by hypothalamic extract in vitro, of the analogues, only Des Gly-NH210 LH-RH ethylamide was degraded. The anterior pituitary gland and kidney extracts failed to degrade [d-Ser6] Des Gly-NH210 LH-RH ethylamide and [d-Ser(But)6] Des Gly-NH210 LH-RH ethylamide as rapidly as LH-RH. Extracts of liver and lung were incapable of catabolizing any of the analogues. There was an inverse correlation between the LH- and FSH-releasing potency of an analogue and its rate of degradation by anterior pituitary gland extract. The slower rates of catabolism of certain analogues of LH-RH by the anterior pituitary gland may explain their increased LH- and FSH-releasing potency.

CHANGES IN RESPONSIVENESS OF DISPERSED PITUITARY CELLS TO LUTEINIZING HORMONE RELEASING HORMONE AT DIFFERENT TIMES OF THE OESTROUS CYCLE OF THE RAT

1981 ◽  
Vol 89 (1) ◽  
pp. 129-134 ◽  
Author(s):  
ALISON SPEIGHT ◽  
G. FINK
Keyword(s):  
Luteinizing Hormone ◽  
Oestrous Cycle ◽  
Female Rats ◽  
Pituitary Cells ◽  
Luteinizing Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Close Relationship ◽  
Specific Receptors ◽  
Lh Rh

Dispersed pituitary cells obtained from female rats with regular oestrous cycles were suspended in Bio-Gel columns and perfused with pulses of luteinizing hormone releasing hormone (LH-RH). There was a close relationship between the amount of LH released and the concentration of LH-RH in the perfusate. It was not possible to elicit the priming effect of LH-RH, but the LH-response changed markedly during the oestrous cycle in a manner similar to that seen in vivo; i.e. the responses of cells prepared from rats killed at pro-oestrus were much greater than the responses of cells prepared from rats killed on other days of the cycle. A similar change in responsiveness was obtained when the columns were perfused with 60 mmol K+/1, suggesting that at least part of the increase in pituitary responsiveness that occurs at pro-oestrus is not dependent upon changes in specific receptors for LH-RH.

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