LUTEINIZING HORMONE RELEASE IN ENTIRE AND CASTRATED RAMS FOLLOWING INJECTION OF SYNTHETIC LUTEINIZING HORMONE RELEASING HORMONE, AND EFFECT OF TESTOSTERONE PROPIONATE PRE-TREATMENT

1975 ◽  
Vol 64 (1) ◽  
pp. 7-16 ◽  
Author(s):  
D. B. GALLOWAY ◽  
J. PELLETIER

SUMMARY Plasma luteinizing hormone (LH) levels and LH responses to intravenous administration of 100 μg luteinizing hormone releasing hormone (LH-RH) were studied in entire rams, long-term castrated animals (operation performed six months previously), long-term castrated animals treated with testosterone for the two preceding weeks and short-term castrated animals (castrated 3 h before LH-RH injection). LH was measured by radioimmunoassay in samples taken at 5 or 15 min intervals. Basal LH levels were lower in entire rams (0·9 ng/ml) than in long-term castrated animals (6·0 ng/ml). After LH-RH treatment the LH response was much smaller (peak level 9·6 ng/ml, total response 13·3 ng/ml/1 h) and slower (120 min to peak) in entire than in long-term castrated animals (peak level 61·8 ng/ml, total response 141·2 ng/ml/1 h, 29 min to peak). Testosterone treatment after long-term castration depressed the basal LH level and delayed the peak LH response after LH-RH to values similar to those for entire rams. After short-term castration the response to LH-RH was already as great (peak level 70·1 ng/ml, total response 133·6 ng/ml/1 h) as after long-term castration. The latency to peak LH level (82 min) was intermediate between that for untreated and testosterone-treated long-term castrated animals (130 min). Testosterone treatment was considered to have acted on the hypothalamus to depress basal levels. The results provided evidence for the presence of two inhibitory actions of the testis at the pituitary level in the ram: a qualitative delaying action of testosterone and a quantitative inhibitory action of the testis on LH release after LH-RH injection. The latter may also be related to plasma testosterone levels.

1977 ◽  
Vol 74 (2) ◽  
pp. 291-296 ◽  
Author(s):  
H. M. FRASER ◽  
J. SANDOW

Immunization against luteinizing hormone releasing hormone (LH-RH) in adult male rats produced a progressive decline in LH and FSH in the circulation to low or non-detectable levels. d-Serine-tertiary-butyl6,des-glycine-NH210 LH-RH ethylamide is an analogue of LH-RH having highly active LH-RH properties in the normal rat. Because it is also immunologically different from LH-RH it can stimulate gonadotrophin release from the anterior pituitary gland of rats immunized against LH-RH without interference from the antibody. The analogue stimulated LH and FSH release in rats 15 weeks after immunization against LH-RH when antibody titre was highest, and after long-term (35 weeks) immunization against LH-RH. d-Serine-tertiary-butyl6,des-glycine-NH210 LH-RH ethylamide and related analogues are therefore potentially useful for reversing the effects of immunization against LH-RH.


1976 ◽  
Vol 71 (1) ◽  
pp. 1-11 ◽  
Author(s):  
G. A. SCHUILING ◽  
H. P. GNODDE

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.


1977 ◽  
Vol 72 (2) ◽  
pp. 121-126 ◽  
Author(s):  
G. A. SCHUILING ◽  
H. P. GNODDE

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.


1976 ◽  
Vol 68 (3) ◽  
pp. 469-474 ◽  
Author(s):  
GWYNETH E. JONES ◽  
KAY BAKER ◽  
DIAN R. FAHMY ◽  
A. R. BOYNS

SUMMARY An injection of luteinizing hormone releasing hormone (LH-RH) increased plasma LH and testosterone concentrations in the male dog, but no significant increase in plasma oestradiol-17β levels was observed. Repeated injections of LH-RH produced an increase in plasma LH levels but there was a progressive decline in the response with each injection. The concentration of plasma testosterone reached a maximum within 40 min of the first injection of LH-RH and remained constant thereafter while plasma oestradiol concentration gradually increased with successive injections of LH-RH.


1982 ◽  
Vol 95 (3) ◽  
pp. 331-NP ◽  
Author(s):  
I. F. W. McDowell ◽  
J. F. Morris ◽  
H. M. Charlton ◽  
G. Fink

Hypogonadal (hpg) mice lack hypothalamic luteinizing hormone releasing hormone (LH-RH); consequently the pituitary gonadotrophs, though differentiated, remain inactive. The acute and chronic responses of gonadotrophs in hpg mice to LH-RH were studied using quantitative electron microscopy, immunocytochemistry for LH and radioimmunoassay of the gonadotrophins. Acute i.v. administration of 40 ng LH-RH to male hpg mice produced an eightfold increase in plasma LH after 5 min, but granule depletion was not detectable ultrastructurally. Vacuoles (300–600 nm) were present more frequently in gonadotrophs from hpg mice given LH-RH compared with control mice. Daily s.c. administration of 2 μg LH-RH to male hpg mice for 20 days stimulated a 63-fold increase in the pituitary content of FSH but only a twofold increase in the pituitary content of LH. Testicular weight increased fivefold but the weight of the seminal vesicles did not change. The frequency of cells immunoreactive for LH increased (× 1·6), the gonadotrophs hypertrophied (× 1·9) and the cell content of granules increased (× 2·3) to values close to the normal range. The rough endoplasmic reticulum and Golgi apparatus became more prominent. A striking result of long-term daily administration of LH-RH was the accumulation of large (1–2 μm) lipid droplets in about 40% of gonadotrophs. All these changes induced by LH-RH regressed towards the untreated hpg state when LH-RH administration was discontinued for 5 and 10 days. These results show that the gonadotrophs of hpg mice can be stimulated trophically by LH-RH, and that long-term administration stimulates the synthesis and release of the gonadotrophins but the effect on FSH is much greater than on LH.


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.


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