CIRCULATING LUTEINIZING HORMONE AND TESTOSTERONE RESPONSE IN RAMS AFTER LUTEINIZING HORMONE RELEASING HORMONE TREATMENT

1974 ◽  
Vol 77 (1) ◽  
pp. 1-9 ◽  
Author(s):  
D. B. Galloway ◽  
Y. Cotta ◽  
J. Pelletier ◽  
M. Terqui

ABSTRACT The relationship between the secretions of LH and testosterone after LH-RH administration was tested in entire rams. Three groups of two rams received, intravenously, 100 μg; 800 μg LH-RH in single injection; or 100 μg × 7 injections at half-hour intervals respectively and samples were collected every 10 or 20 min for 6 hours. Plasma LH and testosterone were assayed by radioimmunoassay. The quantity of LH released following 800 μg LH-RH was higher than released after 100 μg LH-RH and there was a positive correlation between the total amount of LH released after LH-RH and the amount of testosterone released. It seems probable that the pre-injection level of testosterone regulates in a quantitative manner the effect of a given dose of LH-RH. In the case of successive injections of LH-RH, the plasma LH rose to a plateau but the last two treatments failed to prevent the decline in the level of LH. This suggests that testosterone, still high at the time, directly blocked the effect of LH-RH at the level of the pituitary.

1980 ◽  
Vol 58 (6) ◽  
pp. 1100-1104 ◽  
Author(s):  
R. E. Peter

Sexually mature male goldfish, acclimated to 12–14 °C, were injected intraperitoneally with luteinizing hormone – releasing hormone (LH-RH) or the superactive analogue des-Gly10-[D-Ala6]-LH-RH ethylamide (G-A-LH-RH-E). Treatments were a single injection, two injections 12 h apart, and three injections 24 h apart at dosages of 0.1, 0.5, and 1.0 μg/g body weight. Blood samples were taken at 1 or 1.5, 6, and 24 h after the last injection for measurement of serum gonadotropin (GtH) by radioimmunoassay. Serum GtH levels were highest following two injections of LH-RH or G-A-LH-RH-E given 12 h apart; a single injection of the peptides produced the smallest change in GtH levels. The analogue caused a response of longer duration than did LH-RH in certain circumstances. The data also demonstrate that self-potentiation and self-suppression of response can occur under certain treatment conditions with LH-RH and the analogue.


1982 ◽  
Vol 92 (1) ◽  
pp. 141-146 ◽  
Author(s):  
R. L. MATTERI ◽  
G. P. MOBERG

During treatment with cortisol or ACTH, dairy heifers were given two doses of LH releasing hormone (LH-RH) spaced 1·5 h apart. Serum concentrations of cortisol and LH were monitored during each treatment. Treatment with both ACTH and cortisol raised plasma cortisol levels above the respective saline controls (P<0·001). Neither treatment affected basal LH concentrations. A slight depression in LH response was seen in the cortisol-treated animals after the first LH-RH injection, as shown by a statistically significant depression at three of the sample times. There was no significant difference between treated and control LH values after the second LH-RH administration. Treatment with ACTH resulted in significantly reduced LH values at all sample times after both injections of LH-RH.


1974 ◽  
Vol 52 (3) ◽  
pp. 754-758 ◽  
Author(s):  
S. H. Shin ◽  
C. J. Howitt

Several aqueous solvent systems were tested for their efficiency in extracting luteinizing hormone releasing hormone (LH-RH) from rat hypothalamus. Although LH-RH is a water-soluble decapeptide, neutral distilled water extracted only 10% of the LH-RH obtained using acid extraction methods. The efficiency of the acid extraction procedure suggests that in the hypothalamus the releasing hormone is bound to a relatively large molecular weight compound. Using the acidic extraction procedure, we found that hypothalamic LH-RH content is significantly lower in the castrated animal than in the normal rat.


1979 ◽  
Vol 81 (1) ◽  
pp. 109-118 ◽  
Author(s):  
SHUJI SASAMOTO ◽  
SHIGEO HARADA ◽  
KAZUYOSHI TAYA

When 1·0 μg luteinizing hormone releasing hormone (LH-RH) was given i.v. three times at 1 h intervals from 17.00 to 19.00 h on the day of dioestrus (day 0) to regular 4 day cyclic rats, premature ovulation was induced the next morning (day 1) with the number of ova present comparable to normal spontaneous ovulation. The next spontaneous ovulation occurred on the morning of day 5, 4 days after premature ovulation induced by LH-RH. Plasma concentrations of FSH and LH showed transient rises and falls within 1 h of administration of LH-RH; concentrations of FSH in the plasma decreased from 20.00 h on day 0 but markedly increased again from 23.00 h on day 0 to 02.00 h on day 1 and these high levels persisted until 14.00 h on day 1, with only a small increase of plasma LH during this period. The duration of increased FSH release during premature ovulation induced by LH-RH treatment was 6 h longer than the FSH surge occurring after administration of HCG on day 0. Surges of gonadotrophin were absent on the afternoon of day 1 (the expected day of pro-oestrus) and the surges characteristic of pro-oestrus occurred on the afternoon of day 4 and ovulation followed the next morning. The pituitary content of FSH did not decrease despite persisting high plasma levels of FSH during premature ovulation induced by either LH-RH or HCG on day 0. The changes in uterine weight indicated that the pattern of oestrogen secretion from the day of premature ovulation induced by LH-RH to the day of the next spontaneous ovulation was similar to that of the normal 4 day oestrous cycle. When 10 i.u. HCG were given on day 0, an increase in oestrogen secretion occurred on day 2, 1 day earlier than in the group given LH-RH on day 0. This advancement of oestrogen secretion was assumed to be responsible for the gonadotrophin surges on day 3. Similar numbers of fully developed follicles were found by 17.00 h on day 2 after premature ovulation induced by either LH-RH or HCG, suggesting that the shorter surge of FSH during premature ovulation induced by HCG had no serious consequences on the initiation of follicular maturation for the succeeding oestrous cycle in these rats. Administration of LH-RH on day 0 had no direct effect on the FSH surge during premature ovulation. Secretory changes in the ovary during ovulation may be responsible for this prolonged selective release of FSH.


1978 ◽  
Vol 76 (3) ◽  
pp. 487-491 ◽  
Author(s):  
K. YAMASHITA ◽  
M. MIENO ◽  
T. SHIMIZU ◽  
ER. YAMASHITA

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.


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