Stimulation of LH Release and Ovulation in the Rat by Cutaneous Application of Luteinizing Hormone-Releasing Hormone (Lh-Rh) in Dimethyl Sulfoxide (Dmso)

1975 ◽  
Vol 2 (4-5) ◽  
pp. 327-333 ◽  
Author(s):  
J. R. Reel ◽  
R. R. Humphrey ◽  
J. W. Valtkus ◽  
W. C. Dermody
1977 ◽  
Vol 75 (2) ◽  
pp. 277-283 ◽  
Author(s):  
N. BARDEN ◽  
A. BETTERIDGE

The addition of luteinizing hormone releasing hormone (LH-RH) to cultures of monolayers of rat anterior pituitary cells was shown to increase both the concentrations of prostaglandins E1 and E2 (PGE) in the cells and the release of LH over similar ranges of concentrations of LH-RH (10−6 to 10−10 mol/l). The peak concentration of PGE was observed after 2·5 h. The stimulation of the level of PGE in the cells by LH-RH was completely inhibited by two inhibitors of prostaglandin synthetase, which only partially inhibited the stimulation of LH release. Therefore the increased concentration of PGE was not obligatory for the effect of LH-RH on LH release. It was also shown that monobutyryl cyclic AMP stimulated the intracellular concentration of PGE and it is suggested that the stimulation of PGE levels may be mediated by increased levels of cyclic AMP in the cells after the addition of LH-RH.


1976 ◽  
Vol 82 (3) ◽  
pp. 706-709 ◽  
Author(s):  
Gwyneth E. Jones ◽  
A. R. Boyns

ABSTRACT Anterior canine pituitaries were maintained in tissue culture for 8 days, and the immunoreactive prolactin released, was measured by a heterologous radioimmunoassay for canine prolactin. Luteinizing hormone-releasing hormone (LH-RH) and thyrotrophic hormone-releasing hormone (TRH) did not affect prolactin release, while theophylline and oestradiol-17β stimulated the release of canine prolactin.


1978 ◽  
Vol 77 (3) ◽  
pp. 389-395 ◽  
Author(s):  
P. CHANTARAPRATEEP ◽  
M. THIBIER

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 μg). 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 μg 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 < 0·05) reduced by dexamethasone, but on day 2 values in the control and treated groups were similar although significantly (P<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.


1977 ◽  
Vol 55 (1) ◽  
pp. 155-160 ◽  
Author(s):  
Kenneth Ka-Sing Chan

Regressed female medakas were injected with synthetic luteinizing hormone–releasing hormone (LH–RH) intraperitoneally twice a week for 6 weeks under warm temperature (23 ± 1 °C) and short photoperiod (8 h light: 16 h dark). A dose response was observed as shown by the gonadosomatic index and the percentage distribution of class III oocytes with yolk formation. Ovulation also occurred in fish injected with the highest dose. Pituitary cytology revealed stimulation of gonadotropic cells in the proximal pars distalis by synthetic LH–RH at doses of 100 and 1000 ng per gram body weight. Thus, synthetic LH–RH seems to be effective in inducing ovarian development in the medaka. In fish, the presence of a system similar to the mammalian LH–RH system seems likely.


1978 ◽  
Vol 76 (1) ◽  
pp. 49-61 ◽  
Author(s):  
M. B. TER HAAR

SUMMARY The effects of intravenous injection of synthetic luteinizing hormone releasing hormone (LH-RH) on the release of LH and FSH have been studied in the adult guinea-pig. In all the experiments the secretion of FSH was apparently unaffected by administration of LH-RH. The release of LH was log dose-dependent over the range 0·5–50 μg LH-RH. During the female cycle, the maximum increment in the concentration of LH after a single i.v. injection of 0·5 μg LH-RH decreased progressively from day 1 to day 13. Double or triple injections of 1 μg LH-RH at 1 h intervals produced no potentiation on day 3 but progressively greater LH responses occurred on days 7, 10 or 13 of the oestrous cycle. Ovariectomy immediately before the first injection of LH-RH on day 7 blocked the potentiated response to subsequent injections, whereas ovariectomy immediately before the second injection still permitted this potentiation. These results suggest that there is direct ovarian involvement in the potentiated response to LH-RH observed during the later part of the guinea-pig oestrous cycle. Infusion of LH-RH (1 μg over 200 min) produced a potentiated release of LH in female guinea-pigs on day 7 (but not on day 3) of the oestrous cycle after a delay of 1·5 h. It is proposed that there are two 'pools' of LH in the pituitary gland of the female guinea-pig and that the second pool is 'activated' consequent upon previous hypophysial stimulation of secretion from an ovary containing adequately developed follicles.


1979 ◽  
Vol 57 (12) ◽  
pp. 1388-1392 ◽  
Author(s):  
M. Fevre ◽  
D. Jordan ◽  
J. Tourniaire ◽  
R. Mornex

The mechanism of action of adiphenine on in vitro rat anterior pituitary LH release was studied and compared with that of the physiological stimulator luteinizing hormone releasing hormone (LH-RH) on LH release. The comparative study showed that adiphenine and LH-RH were able to increase medium LH concentration in a dose-dependent manner and had similar time courses of action between 1 and 4 h incubation. However, there were several main differences between the effects of adiphenine and LH-RH. The adiphenine action was not calcium dependent, was inhibited in a high K+ medium concentration, and was substituted after energy depression. It is concluded that adiphenine probably acts near the ultimate steps of the LH release pathway and could be a useful pharmacological tool for studying the mechanism of LH release.


1974 ◽  
Vol 61 (1) ◽  
pp. 123-131 ◽  
Author(s):  
GWYNETH E. JONES ◽  
A. R. BOYNS

SUMMARY Intravenous injections of synthetic luteinizing hormone releasing hormone (LH-RH) stimulated LH secretion in male dogs. An i.m. injection of 0·025–2·5 mg oestradiol-17β given 2·5 h but not 24 h before administration of LH-RH blocked LH secretion. Diethylstilboestrol (2·5 mg) also blocked LH secretion but meso-dihydrodibutylstilboestrol (2·5 mg) was without effect. Testosterone (2·5 and 25 mg), dihydrotestosterone (2·5 mg), 5α-androstane-3α, 17β-diol (2·5 mg), 5α-androstane-3β, 17β-diol (2·5 mg), 5α-androstane-3α, 17α-diol (0·125 mg), 5α-androstane-3β, 17α-diol (0·125 mg) and progesterone (25 and 50 mg) did not prevent LH-RH stimulation of LH secretion.


1977 ◽  
Vol 72 (1) ◽  
pp. 59-67 ◽  
Author(s):  
D. B. CRIGHTON ◽  
J. P. FOSTER

SUMMARY Anoestrous ewes were given two injections of 30 μg 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 μg 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 area 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.


1977 ◽  
Vol 73 (3) ◽  
pp. 519-527 ◽  
Author(s):  
G. A. LINCOLN

SUMMARY Six adult Soay rams were subjected to an artificial lighting régime of alternating 4 month periods of long days (16 h light: 8 h darkness) and short days (8 h light: 16 h darkness) which induced a seasonal cycle in testicular development and regression during a period of 32 weeks. On 15 occasions during the study pituitary responsiveness was assessed by measuring the concentration of luteinizing hormone (LH) in jugular blood samples collected at frequent intervals after the intravenous injection of 1 pg synthetic luteinizing hormone releasing hormone (LH-RH). It was shown that both the magnitude and duration of the induced release of LH changed in relation to the photoperiod; the magnitude was greatest during long days when the rams were sexually quiescent, while the duration of the LH release was greatest during short days at the peak of testicular activity. This pattern of responsiveness was modified by implantation of the rams with testosterone.


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