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PubMed1976

Effect of luteinizing hormone releasing hormone on plasma levels of luteinizing hormone, oestradiol and testosterone in the male dog.

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-17beta 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.

Animals↗

PubMed1976

Secretion of luteinizing hormone caused by continuous infusions of luteinizing hormone releasing hormone in the long-term ovariectomized rat: effect of oestrogen pretreatment.

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 ple maintained for the rest of the experiment (9h). 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 mug 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.

Animals↗

PubMed1977

Luteinizing hormone release after two injections of synthetic luteinizing hormone releasing hormone in the ewe.

Anoestrous ewes were given two injections of 30 mug synthetic luteinizing hormone releasing hormone (LH-RH) separated by one of the following intervals: 1-5, 3, 6, 12 or 24 h. The first injection caused an increase in the plasma LH concentration in each animal. The response to the second injection was dependent on the interval between the injections. When the second injection was administered 1-5 h after the first it caused a further increase in the LH concentration to maximal levels which were significantly greater than those induced in the other anoestrous groups. When the second injection was administered 3 h after the first, there was no significant difference between the responses to the two injections although the time to reach the maximal LH concentration was shorter and the height of the LH peak was greater in each animal following the second injection. When the second injection was administered 6, 12 or 24 h after the first, the LH response was significantly less, in terms of height and area of the induced peak, than following the first injection. The LH response to the second injection was particularly low in the 12 and 24 h groups. Two injections of 30 mug synthetic LH-RH were also administered at 1-5 h intervals to ewes on either day 10 of the oestrous cycle or at onset of oestrus. The pattern of LH responses in all these animals was similar to that observed in anoestrous ewes injected at 1-5 h intervals. The total LH release, as assessed in terms of the induced peaks, was significantly greater in the onset of oestrus group than in the day 10 group or any of the anoestrous groups. Presumably the sensitization-desensitization sequence of the pituitary gland to LH-RH which has been demonstrated, together with the effects of sex steroid hormones, must play an important part in the development and decay of the natural preovulatory LH peak.

Anestrus↗

PubMed1977

Gonadotrophin release by a highly active analogue of luteinizing hormone releasing hormone in rats immunized against luteinizing hormone releasing hormone.

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.

Animals↗

PubMed1978

Steroid priming of the luteinizing hormone response to luteinizing hormone releasing hormone.

Perifusion experiments were performed to study the stimulatory effects of luteinizing hormone releasing hormone (LH-RH) on the release of LH from anterior pituitary tissue. Exposure of pituitary tissue from normal male rats to LH-RH (5 ng/ml for 5 min) induced a small release of LH; in tissue from ovariectomized rats receiving no pretreatment, the release was more than three times greater and in tissue from gonadectomized male or female rats pretreated with oestradiol benzoate and progesterone, the release was six times greater than that observed in normal rats. Further exposure of pituitary tissue from gonadectomized steroid-pretreated male and female rats to LH-RH (5 ng/ml) induced an increase in the level of LH even greater than that seen after the initial exposure (priming action of LH-RH); in tissue from ovariectomized rats receiving no pretreatment, less LH was released than after the first exposure to LH-RH and in tissue from normal male rats the response was unchanged.

Animals↗

PubMed1978

Effects of dexamethasone on the responses of luteinizing hormone and testosterone to two injections of luteinizing hormone releasing hormone in young postpubertal bulls.

Six young postpubertal bulls were studied in two experiments, 3 months apart. In experiment 1, three bulls received i.m. injections of dexamethasone (20 mg) and 5 h later these animals plus three control bulls received i.m. injections of luteinizing hormone releasing hormone (LH-RH, 250 microgram). In experiment 2, the controls from experiment 1 received dexamethasone and the treated animals from experiment 1 acted as controls for experiment 2. All bulls also received an i.m. injection of 250 microgram LH-RH on day 2 of each experiment. The concentrations of LH and testosterone in samples of jugular blood were determined by radioimmunoassay. There were no significant differences in the patterns of testosterone and LH release between the two experiments. On day 1, the response of LH to LH-RH was significantly (P less than 0.05) reduced by dexamethasone, but on day 2 values in the control and treated groups were similar although significantly (P less than 0.05) lower than values on day 1. The response of testosterone to LH-RH was not affected by dexamethasone. These results are discussed in terms of the site of action at which dexamethasone may act to depress the release of LH.

Animals↗

PubMed1979

Differential control of luteinizing hormone and follicle-stimulating hormone by luteinizing hormone releasing hormone in the ram.

Adult Soay rams with low concentrations of gonadotrophins in the circulation as a result of 12 weeks of exposure to long daylengths (16 h light : 8 h darkness) were given small doses (100 ng) of synthetic luteinizing hormone releasing hormone (LH-RH) into the jugular vein two, four or seven times/day for 10 days. Each injection of LH-RH induced a transitory increase in the concentration of LH and testosterone in the plasma, whereas the concentration of FSH showed little immediate change. After repeated treatment with pulses of LH-RH, the responses of LH and testosterone became slightly enhanced and the plasma concentration of FSH became permanently raised; these changes were most conspicuous in the animals receiving the most frequent injections. At the end of the study when the injections of LH-RH were stopped, the concentrations of LH and testosterone remained low but the concentrations of FSH continued to be maintained at a high level for at least 24 h.

Animals↗

PubMed1979

Suppression of the luteinizing hormone releasing effect of luteinizing hormone releasing hormone by arginine-vasotocin.

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 microgram/kg body wt) caused no significant alterations in the testicular output of 17-oxosteroids. The administration of LH-RH (5 microgram/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 microgram/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 microgram/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 acting directly on the anterior pituitary gland.

17-Ketosteroids↗

PubMed1983

Luteinizing hormone releasing hormone prevents testicular atrophy in golden hamsters exposed to a short photoperiod: temporal difference in effectiveness of administration of luteinizing hormone releasing hormone.

Exposure of male golden hamsters to short photoperiods of 6 h light: 18 h darkness led to testicular and accessory sex organ atrophy in 5 weeks. Short photoperiods also significantly depressed serum levels of LH, FSH, prolactin and testosterone in samples obtained by decapitation, but not in samples collected on the preceding day under ether anaesthesia. Injections of luteinizing hormone releasing hormone (LH-RH) at 09.00 h (lights on) or at 15.00 h (lights off) prevented testicular regression when compared with hamsters receiving injection vehicle only. However, the hamsters receiving LH-RH injections at lights on had significantly greater testicular weight and accessory sex organ (seminal vesicles and coagulating glands) weight and testosterone concentration than those receiving LH-RH at lights off. No increase in testicular weight was observed in hypophysectomized male hamsters given the same LH-RH injections and the same lighting regimen. These results indicate that LH-RH alone can prevent, at least partially, testicular and sex organ atrophy and increase serum testosterone concentration by stimulating release of LH and FSH in hamsters exposed to short photoperiods, involving temporal difference of LH-RH action. Further implications of the results are discussed.

Animals↗

PubMed1982

Effect of dosage and frequency of injection of luteinizing hormone releasing hormone on release of luteinizing hormone and follicle stimulating hormone in estradiol-treated steers.

The objective was to determine how estradiol (0 vs 1 mg) and changes in the dosage of luteinizing hormone releasing hormone (LHRH; 1,000 ng/steer vs 1 ng/kg body weight) and frequency of LHRH injection (25 vs 50 min) affect LH and follicle stimulating hormone (FSH) release in steers. In steers pretreated with estradiol peak concentrations of LH in serum after LHRH averaged 14.4 ng/ml, which was greater (P less than .001) than peak concentrations in steers given oil (7.4 ng/ml). Increasing the dosage of LHRH from 1 ng/Kg body weight (approximately or equal to 300 ng/steer) to 1,000 ng/steer increased (P less than .001) peak LH values from 7.5 to 14.4 ng/ml. Furthermore, increasing the frequency of LHRH injections from once every 50 min to once every 25 min increased (P less than .001) LH release, but only in steers given estradiol. Estradiol reduced basal concentrations of FSH by 65% and then increased LHRH-induced FSH release by 276% (P approximately .07) relative to values for steers given oil. Only when 1,000 ng LHRH was given every 25 min to steers pretreated with estradiol were LH and FSH release profiles similar to the preovulatory gonadotropin surges of cows in magnitude, duration and general shape. The results demonstrate that increases in the dosage or frequency of LHRH pulses increase LHRH-induced release of LH, but not of FSH. Furthermore, these results are consistent with the hypothesis that in cows, estradiol increases responsiveness of the gonadotrophs to LHRH and then increases the magnitude and frequency of pulses of LHRH secretion beyond basal levels, thereby causing the preovulatory gonadotropin surges.

Animals↗

PubMed1986

Effects of restriction of dietary energy intake during the prepubertal period on secretion of luteinizing hormone and responsiveness of the pituitary to luteinizing hormone-releasing hormone in heifers.

The working hypothesis that a low plane of nutrition during the prepubertal period delays puberty in heifers by retarding the prepubertal increase in secretion of luteinizing hormone (LH) was investigated. Secretion of LH and the responsiveness of the pituitary to LH-releasing hormone (LHRH) were compared in heifers fed a growing diet (which allowed spontaneous occurrence of puberty; n = 12; control) or an energy deficient diet (which delayed puberty; n = 11; delayed) during the prepubertal period. The dietary treatments were initiated when the heifers were 299 +/- 14 (mean +/- SD) d of age (d 0 of the experiment) and continued until d 175 of the experiment (474 +/- 14 d of age). Weight gains were .79 +/- .05 (mean +/- SE) and .21 +/- .03 kg X head-1 X d-1 for control and delayed heifers, respectively. Puberty occurred on d 120 +/- 14 of the experiment (428 +/- 13 d of age) in control heifers, whereas none of the delayed heifers attained puberty during the feeding period. Serum concentration of LH and the frequency of LH pulses increased rapidly during the 175-d feeding period in control heifers. In delayed heifers, serum LH concentration increased less rapidly and no increase in pulse frequency was detected during the experimental period. Amplitude of LH pulses tended to be higher in control than delayed heifers. Responsiveness of LH secretion to LHRH was lower in delayed than control heifers. It is speculated that failure of secretion of LH to increase is the causative factor for delayed puberty when dietary energy is limited during the prepubertal period in heifers.

Animals↗

PubMed1989

Luteinizing hormone concentrations in serum of postpartum beef cows injected with microencapsulated luteinizing hormone-releasing hormone analog.

Twenty-five cows were divided equally into five groups to determine whether [D-Trp6]-luteinizing hormone releasing hormone (LHRH-A) microencapsulated in poly (DL-lactide co-glycolide) would increase basal serum concentrations of LH during the postpartum period. On d 5 postpartum, cows were injected i.m. with 2 ml of vehicle alone (Group 1) or vehicle containing microcapsules calculated to release .4, 1.6, 6.4 or 25.6 micrograms LHRH-A per day for approximately 30 d (Groups 2, 3, 4 and 5, respectively). Cows were bled every 15 min for 4 h immediately before and after injection and every 15 min for 4 h at weekly intervals for the next 4 wk to evaluate serum profiles of LH. Estrus was determined by twice daily observations and confirmed by serum progesterone. More cows in Groups 2, 3, 4 and 5 exhibited pulsatile patterns of LH after LHRH-A injection than in Group 1 (P less than .06). More pulses of LH were observed after LHRH-A injection in Groups 4 and 5 than in Group 1 (P less than .01). Mean concentrations of LH within treatment groups did not change during the initial injection, except in Group 5. All cows in Group 5 had a surge of LH immediately after injection. The induced surge of LH in two cows in Group 5 cows resulted in progesterone profiles similar to those during a normal luteal phase. Days to first postpartum estrus were not different among the five treatment groups. Microencapsulated LHRH-A given at a dose estimated to release 25 micrograms LHRH-A/d was effective in elevating LH concentrations following injection. However, effectiveness of this hormonal treatment in shortening postpartum anestrus was not substantiated.

Anestrus↗

PubMed1983

Luteinizing hormone release and androgen production of avian hybrids in response to luteinizing hormone releasing hormone injection.

The levels of luteinizing hormone (LH) and androgens were measured in sterile avian hybrids. Guinea fowl-chicken and peafowl-guinea fowl hybrids were bled before and after injection with LH- releasing hormone (LHRH). The preinjection LH levels for the guinea fowl-chicken hybrids were below or at the very lower limit of the assay sensitivity and the peafowl-guinea fowl hybrids averaged 1.3 ng/ml. Within 10 min after LHRH injection, LH had increased dramatically in both hybrids and then began to slowly decline. Androgen levels in the guinea fowl-chicken hybrids increased from 16.2 pg/ml to 95.2 pg/ml and continued to increase, reaching 287 pg/ml at the last bleeding 60 min after injection.

Androgens↗

PubMed1985

Ovine luteinizing hormone-induced steroid and luteinizing hormone secretion, and ovulation in intact and pregnant mare serum gonadotropin-primed hens.

Studies were conducted to investigate the effect of ovine luteinizing hormone (LH) treatment on steroid and LH secretion and ovulation in intact, saline-primed hens and in pregnant mare serum gonadotropin (PMSG)-primed hens. Intact, saline-primed hens, injected 12 hr prior to the first (C1) ovulation of the sequence, responded with fully potentiated preovulatory surges of progesterone (P4) (peak value was 371% above preinjection values), estradiol-17 beta (E2) (117% above baseline), LH (220% above baseline), and premature ovulation. By comparison, those hens injected at the same time prior to the second (C2) ovulation responded with a lesser increase in plasma P4 (peak value was 305% above baseline) and E2 (72% above baseline), and there was no significant increase in plasma LH. Within this group, 4 of 5 hens failed to ovulate prematurely. All groups of PMSG-primed hens had significantly higher preinjection concentrations of P4 and E2, and lower basal concentrations of LH, compared to saline-primed hens. Subsequent to treatment of PMSG-primed hens with 25 or 100 micrograms ovine LH, there was a significant increase in plasma P4 to approximately 200% above preinjection concentrations. By contrast, there was a nonsignificant increase in plasma LH (50% above baseline values) and no significant increase in plasma E2. The ovulatory response following PMSG-priming was greatest in hens injected with 100 micrograms ovine LH (5 of 5 hens ovulated), while 3 of 5 hens injected with 25 micrograms ovine LH and 6 of 6 saline-challenged hens failed to ovulate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Alcohol effects on luteinizing hormone-releasing hormone-stimulated luteinizing hormone and follicle-stimulating hormone in female rhesus monkeys.

The effects of acute alcohol administration on anterior pituitary function were studied in eight female rhesus monkeys during the follicular phase of the menstrual cycle. Integrated plasma samples were collected for 80 min before and 120 min after nasogastric intubation of alcohol (2.5 or 3.5 g/kg) or isocaloric sucrose control solution. Synthetic luteinizing hormone-releasing hormone (LHRH; 100 micrograms i.v.) was then administered, and plasma samples were collected for an additional 180 min. After sucrose control administration, LHRH stimulated a significant increase in both LH (P less than .001) and follicle-stimulating hormone (FSH) (P less than .004) within 30 and 80 min, respectively. After alcohol administration, LHRH-stimulated LH increased significantly (P less than .001) within 15 min when blood alcohol levels averaged 184 ( +/- 14.3) and 276 ( +/- 14.9)mg/dl. However, FSH levels remained equivalent to base line after alcohol and LHRH administration. The prevention by alcohol of LHRH stimulation of FSH during the follicular phase suggests that alcohol may attenuate normal follicular maturation, which in turn could result in luteal phase inadequacy or anovulation, conditions often observed in alcohol-dependent women and in animal models of alcoholism.

Animals↗

PubMed1988

The effect of luteinizing hormone on parturition in rats; imidazole antifungals may affect parturition via luteinizing hormone.

Studies were carried out to investigate the mechanism whereby the imidazole anti-fungal, tioconazole, affects parturition in rats. Administration s.c. of luteinizing hormone (LH) to pregnant rats on days 15-17 post-insemination (p.i.) or days 15-21 p.i. delayed the onset of parturition by a day and markedly reduced the ovarian production of 17 beta-estradiol, but not of progesterone. Administration of LH on days 18 and 19 p.i., which was already known to advance birth, reduced ovarian production of progesterone, but not of 17 beta-estradiol. The similarity of these results to those for tioconazole administered from days 15 p.i. or on days 18 and 19 p.i. suggests that tioconazole affects parturition in rats, at least in part, via LH.

Animals↗

PubMed1983

Expression of alpha subunit and luteinizing hormone beta genes in the ovine anterior pituitary. Estradiol suppresses accumulation of mRNAS for both alpha subunit and luteinizing hormone beta.

Bovine cDNA clones containing coding sequences for growth hormone, prolactin, alpha subunit, and luteinizing hormone beta (LH beta) have been used to quantitate their respective mRNA concentrations in anterior pituitary glands isolated from ovariectomized ewes, or from ovariectomized ewes treated for three weeks with estradiol. Concentrations of mRNAs for prolactin or growth hormone remained unchanged in either physiological state. In contrast, treatment with estradiol resulted in a 98% decrease of mRNA for LH beta, relative to untreated animals. This change in mRNA was associated with a similar decrease in the concentrations of pituitary and serum LH. Administration of estradiol also led to a reduction (86%) of alpha subunit mRNA. These results suggest that estrogen regulates the expression of the genes encoding both the alpha and LH beta subunit prior to translation. Furthermore, the pronounced effect of estradiol on the concentrations of mRNAs for alpha subunit and LH beta suggest that the assembly of mature glycoprotein hormones may not be limited solely by the rate of accumulation of the beta subunit.

Animals↗

PubMed1976

Prolonged anti-luteinizing hormone/follicle-stimulating hormone-releasing activities of some synthetic antagonists of luteinizing hormone-releasing hormone.

A number of synthetic analogs of luteinizing hormone-releasing hormone (LH-RH) were screened for their in vivo antigonadotropin-releasing activities using a four-point bioassay test in immature male rats. Of the peptides tested, the most effective were those containing D-phenylalanine in position 2 of the decapeptide chain in conjunction with D-leucine or, preferably, D-phenylalanine in position 6. Several inhibitory peptides that were found to be very potent were reassayed and compared for duration of inhibition in immature male rats, whereupon the D-Phe2 analogs were found to be particularly long-acting. The most active and persistent peptide of the series, [D-Phe2, D-Phe6]-LH-RH, was able to inhibit the response to exogenous LH-RH for up to 6 hours after its injection.

Animals↗