Effect of oestradiol benzoate or luteinizing hormone on levels of progesterone in the pseudopregnant rat

1982 ◽  
Vol 94 (3) ◽  
pp. 369-379 ◽  
Author(s):  
W. J. de Greef ◽  
J. Th. J. Uilenbroek ◽  
F. H. de Jong

The present study was concerned with a possible involvement of LH in the process of functional luteolysis in the pseudopregnant rat. Daily injections with 2 μg ovine LH during pseudopregnancy reduced peripheral and ovarian levels of progesterone in intact and hysterectomized rats and in hypophysectomized rats with a pituitary transplant under the kidney capsule. However, a daily dose of 10 μg LH did not alter the levels of progesterone. A short-lasting decrease in plasma progesterone occurred when endogenous levels of LH were temporarily raised in pseudopregnant rats by a single injection of LH releasing hormone (LH-RH). Treatment with LH or LH-RH, however, did not shorten the duration of pseudopregnancy. Daily treatment of pseudopregnant rats with 5 or 20 ng oestradiol benzoate, but not with 1000 ng, decreased plasma levels of progesterone. On the other hand, daily treatment with oestradiol benzoate did not affect plasma progesterone in pseudopregnant rats which were hypophysectomized and had an ectopic pituitary gland. Plasma levels of LH were not increased in the animals receiving 5 or 20 ng oestradiol benzoate daily, suggesting that the effect of oestradiol benzoate on plasma progesterone is not through an enhanced secretion of LH. Treatment with oestradiol benzoate did not affect the duration of pseudopregnancy. In conclusion, low doses of LH can reduce peripheral levels of progesterone during pseudopregnancy, but it seems improbable that LH is involved in the process of functional luteolysis. Furthermore, low doses of oestradiol benzoate can also decrease plasma progesterone, but the mechanisms involved are still not understood.

1983 ◽  
Vol 97 (3) ◽  
pp. 327-338 ◽  
Author(s):  
W. J. de Greef ◽  
F. H. de Jong ◽  
J. de Koning ◽  
J. Steenbergen ◽  
P. D. M. van der Vaart

Steroid-free bovine follicular fluid (bFF) selectively suppresses the plasma levels of FSH in the female rat, demonstrating that bFF contains inhibin-like material. The present study was concerned with the effects of bFF on the hypothalamic release of LH releasing hormone (LH-RH) into hypophysial stalk blood and on the metabolic clearance rates of gonadotrophins. The metabolic clearance rates of FSH, LH and prolactin were determined after a single injection of and during a constant infusion with adenohypophysial extract. Similar results were obtained with both methods, and treatment with bFF did not alter the metabolic clearance rates of FSH, LH and prolactin. Anaesthesia with urethane, used for surgery involved in the collection of hypophysial stalk blood, did not interfere with the effect of bFF on plasma levels of FSH. The administration of bFF did not change the hypothalamic content of LH-RH, but caused a 30% decrease in the levels of LH-RH in hypophysial stalk plasma. However, a fraction isolated from bFF, which contained 20 times more inhibin-like activity per mg protein than bFF, did not alter the hypothalamic release of LH-RH into the hypophysial portal blood while this fraction was effective in specifically suppressing the plasma levels of FSH. It was concluded that the inhibin-like activity in bFF does not suppress the plasma levels of FSH by affecting its plasma clearance or by influencing the hypothalamic release of LH-RH, but that it has a direct effect on the adenohypophysis in inhibiting the release of FSH. Besides the inhibin-like activity, bFF also contains another factor which can decrease the levels of LH-RH in hypophysial stalk plasma.


1981 ◽  
Vol 90 (1) ◽  
pp. 41-51 ◽  
Author(s):  
J. A. F. TRESGUERRES ◽  
A. I. ESQUIFINO

Male and female Wistar rats were made hyperprolactinaemic by grafting two pituitary glands of litter-mate donors under the kidney capsule at 30 days of age. Other animals were sham-operated at the same age to serve as controls. Plasma levels of prolactin, LH and FSH were measured by double-antibody radioimmunoassay. Basal preoperative prolactin levels of ∼ 10 ng/ml increased after the transplantation in both male and female rats, reaching values of ∼ 180 ng/ml. Levels of LH were significantly reduced in these hyperprolactinaemic rats, whereas an increase in FSH values was seen. After administration of LH releasing hormone (LH-RH) a reduced LH response was seen but there was no response of FSH to LH-RH or even a decrease in FSH values. Prolactin levels were also reduced by LH-RH injection. Although an increase in prolactin levels was observed in control animals after a challenge with oestradiol benzoate, reduced increments were seen in experimental animals. The positive feedback effect of oestradiol benzoate on LH in females was reduced in pituitary-grafted rats but a potentiation of the FSH positive feedback could be clearly detected. This study suggests a dissociation of LH and FSH regulation in hyperprolactinaemia.


1984 ◽  
Vol 103 (3) ◽  
pp. 301-309 ◽  
Author(s):  
G. A. Schuiling ◽  
N. Pols-Valkhof ◽  
G. C. J. van der Schaaf-Verdonk ◽  
T. R. Koiter

ABSTRACT The LH and FSH release-stimulating (experiment 1) and -blocking (experiment 2) effects of LH-releasing hormone (LHRH) and of the LHRH analogue d-Ser(But)6-des-Gly10-LHRH-ethylamide (buserelin), as well as the effect of combined treatment with LH RH and oestradiol benzoate (OB; experiment 3) on the 'supra-maximally' LHRH-stimulated release of LH and FSH were studied in rats ovariectomized for 2 weeks. Pretreatment with LHRH (250 or 500 ng/h) or buserelin (250 ng/h) for 6 days was effected by means of subcutaneously implanted Alzet osmotic minipumps; control rats received a 'sham pump', i.e. a piece of silicone elastomer with the dimensions of a minipump. Oestradiol benzoate (3 μg/injection) or solvent was injected subcutaneously 75 and 27 h before the induction of LH/FSH responses. Experiment 1 revealed that after infusion of LHRH and buserelin, both at the rate of 1 μg/h, plasma LHRH concentrations were established which were about twice as low as the plasma buserelin concentrations. This might suggest that buserelin has a longer half-life than LHRH. As an LH and FSH release-stimulating substance, however, it appeared that buserelin was about as effective as LHRH. Experiment 2, however, suggested that as an LH/FSH release-blocking agent buserelin was much more effective than LHRH. In addition, after buserelin pretreatment the pituitary glands contained much less LH and FSH than after LHRH pretreatment at both dose levels used. However, this may also (at least partly) be due to the fact that buserelin has a longer half-life so that after infusion of buserelin and LHRH at the same rate the plasma concentrations of buserelin are higher than those of LHRH; after buserelin infusion the pituitary gland is therefore stimulated at a higher intensity. Experiment 3 showed that in OB-injected, sham-implanted rats the LHRH-stimulated secretion of LH and FSH was significantly higher than in the oil-injected, sham-implanted rats. In the LHRH-pretreated rats (LHRH: 250 ng/h for 6 days), however, the already depressed LHRH-stimulated secretion of LH and FSH was still further depressed by OB treatment. These latter results suggest that the increase of the pituitary LHRH responsiveness during exposure to oestrogen requires a reduction of the LHRH stimulation, which is normally caused by the negative feedback of oestrogen on the hypothalamus. J. Endocr. (1984) 103, 301–309


1972 ◽  
Vol 71 (3) ◽  
pp. 551-556 ◽  
Author(s):  
Ulf Larsson-Cohn ◽  
Elof D. B. Johansson ◽  
Leif Wide ◽  
Carl Gemzell

ABSTRACT Daily determinations of the plasma level of progesterone and the urinary excretion of LH and oestrogens were performed in four women during one control cycle followed by three months of daily treatment with 0.1 mg of norethindrone. According to the plasma progesterone pattern, all four women seemed to ovulate during their control cycle. Two women became pregnant during their second cycle of treatment. During treatment all four women showed an atypical LH pattern without any distinct midcycle peak. The mean LH excretion during treatment was not significantly different from the mean level of follicular phase of normal cycles. The oestrogens and progesterone levels were within normal ranges. It is concluded that during treatment with 0.1 mg of norethindrone daily an apparently normal pregnancy may occur in spite of a different LH excretion pattern.


1977 ◽  
Vol 84 (1) ◽  
pp. 45-50 ◽  
Author(s):  
E. V. YoungLai

ABSTRACT Experiments were performed in the rabbit to determine whether 20α-hydroxy-4-pregnen-3-one (20-OHP) can maintain luteinizing hormone (LH) secretion after injections of LH-releasing hormone (LH-RH). Female rabbits were castrated at least 2 weeks prior to investigation. On the day before LH-RH injection they were cannulated and a dose of oestradiol benzoate (OeB), 100 μg/kg, given intramuscularly. LH-RH, 500 ng/kg, was injected as a bolus via the cannula and 20-OHP, 100 μg/kg and 2.5 mg/kg, injected intramuscularly immediately after. Blood was withdrawn at intervals for up to 5½ h after LH-RH injection. LH secretion dropped to pre-stimulation levels within 3 h after LH-RH alone or in combination with 20-OHP. Administration of LH-RH to oestrogen primed intact females also gave a peak of LH which returned to pre-stimulation levels within 3 h. However, mating seemed to maintain LH levels for a greater period of time.


1982 ◽  
Vol 92 (3) ◽  
pp. 419-424 ◽  
Author(s):  
P. J. B. ANDERSON ◽  
A. E. FATINIKUN ◽  
A. D. SWIFT

Concentrations of testosterone were measured daily in plasma of neonatal male rats from the day of birth for 7 days. It was found that a significant (P <0·001) increase in mean plasma levels of testosterone occurs on day 2 of life, followed by a decrease on day 3. Separation of male rat pups from their mothers on the second day of life for as little as 2 h was associated with a significant (P <0·001) fall in plasma testosterone concentration. Hand-feeding the pups with a proprietary human milk substitute (milk-replacer) from birth until the expected time of the testosterone peak resulted in no increase in plasma levels of testosterone; inclusion of an antiserum to LH-releasing hormone (LH-RH) in the milk-replacer decreased the testosterone levels as did removing any supposed endogenous LH-RH in the milk replacer. Addition of a highly potent analogue of LH-RH, either in the presence or absence of the LH-RH antiserum, to the milk-replacer resulted in mean plasma levels of testosterone similar to those in naturally suckled rats. Rats fed with human milk showed an increase in plasma levels of testosterone. It is concluded that the increase in the plasma testosterone concentration found in male rat pups on the second day of life, which may have an important effect on the organization of the brain, is provoked indirectly by LH-RH ingested during suckling.


1972 ◽  
Vol 70 (1) ◽  
pp. 167-174 ◽  
Author(s):  
Artur Ber

ABSTRACT Hypophysectomy was performed at the same time as ovariectomy in 19 rats aged 6 weeks; in addition a fragment of the animal's own ovary was implanted into the greater omentum. The graft took but there was complete cessation of the growth of the implant and a decrease in body and uterine weights as compared to 15 ovariectomized controls of the same age killed after one month. This shows that the pituitary is indispensable for the growth of ovarian implants but not for their take. In 84 spayed rats aged 3 weeks with ovarian implants, methallibure (6 mg/day in a 0.2% solution of Tween 20) was given by gavage during one month. Some of them were treated with PMSG (20 IU/day), HCG (20 IU/day) or with oestradiol benzoate (0.05 mg/day) only or in combinations. As controls, there were 74 spayed rats with ovarian implants, seven of which received Tween 20, and 67 were untreated. No differences were found between the two control groups. Methallibure alone caused arrest of the development of the implants and uteri and a decrease in body weight. In the methallibure treated animals HCG stimulated the growth of the implant which was, however, smaller than that in the controls, while PMSG restored the weight of the implant even above that of the control rats. Oestradiol benzoate caused a further diminution in the size of the implants but augmented considerably the influence of HCG on the implants. It had no effect on the weight of the implant in rats treated with PMSG. It is concluded that FSH is the principal implant growth-promoting factor and that oestrogens appear to act in two directions. They decrease the gonadotrophin output from the pituitary thus inhibiting the growth of the implants, but in the presence of gonadotrophins they act directly on the implants, promoting their development.


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.


1983 ◽  
Vol 98 (1) ◽  
pp. 7-17 ◽  
Author(s):  
R. F. Walker

In ovariectomized rats treated chronically with oestrogen there is a loss of positive feedback effects on LH secretion. This was not due to depletion of pituitary LH since injection of LH releasing hormone (LH-RH; 50 ng/100 g body wt) caused a significant (P < 0·01) rise in serum LH even after the loss of spontaneous LH surges. However, the magnitude of the increase in serum LH in response to LH-RH was greater (412 ± 41 μg/l) before than after (291 ± 29 μg/l) loss of the LH surges. Excessive blood sampling was also not responsible, since positive feedback responses declined comparably in rats bled daily or once every 3–4 days. Progesterone (0·5 mg s.c.), administered for 5 consecutive days, failed to restore LH surges indicating that deficiency of this steroid after ovariectomy does not cause positive feedback responses to disappear in rats exposed chronically to oestrogen. Moreover regular daily fluctuations in serum progesterone, probably of adrenal origin, occurred before as well as after daily LH surges were lost. Serotonin content and turnover were depressed (P < 0·05) when ovariectomized rats first received the subcutaneous capsules containing oestrogen. This change correlated temporally with the onset of daily LH surges and was eventually lost. After 30 days exposure to oestrogen, serotonin turnover increased (P < 0·01) and positive feedback responses were absent. Catecholamine levels and turnover did not show differential responses to oestrogen and were depressed after acute as well as chronic steroid treatment. p-Chlorophenylalanine (pCPA; 250 mg/kg)+ l-dihydroxyphenylalanine (l-DOPA; 200 mg/kg), which depress serotonin and enhance catecholamine synthesis respectively, failed to reinstate LH surges, but these were restored in 22% of the rats receiving l-DOPA alone. pCPA, followed 2 days later by 5-hydroxytryptophan (5-HTP) at 11.00 h, reinstated LH surges in 88% of rats, and a dose–response curve showed that as little as 4 mg 5-HTP/kg stimulated repetitive LH surges when given with pCPA according to this schedule. However, the administration of α-methyl-p-tyrosine + l-DOPA, an analogous treatment involving catecholamines, was only marginally effective (15%). These findings suggest that perturbations of monoamine metabolism occurring in ovariectomized rats exposed to oestrogen for several weeks contribute to loss of daily LH surges. Since pCPA + 5-HTP restored LH surges most effectively, then positive feedback may disappear as the facilitatory effect of serotonin is lost after chronic oestrogen administration.


1982 ◽  
Vol 92 (3) ◽  
pp. 327-339 ◽  
Author(s):  
E. TERASAWA ◽  
J. NOONAN ◽  
W. E. BRIDSON

Although the anterior pituitary gland has been shown to be a site of oestrogen feedback in the non-human primate, the role of the hypothalamus as a site of ovarian steroid feedback in facilitating gonadotrophin release has not been ruled out. In the present study, LH release in response to 2·5 mg progesterone with oestradiol benzoate (OB; 10 μg or 30 μg) 30 h earlier was observed in the ovariectomized monkey. Then pentobarbitone sodium was administered to block the progesterone-induced LH response. Serum levels of LH, oestradiol (OE2) and progesterone were measured by radioimmunoassay. In the first series of experiments a group of nine rhesus monkeys received subcutaneous implants of a small silicone elastomer capsule containing OE2. Two weeks later, either OB and oil, or OB and progesterone were injected sequentially. Oestradiol benzoate (10 μg) followed by oil 30 h later failed to cause any clear LH release, while 30 μg OB followed by oil induced a single peak of LH release with a peak latency of 16·5 ± 1·9 (s.e.m.) h after oil, and a duration of 69·8 ± 10·2 h. Regardless of the dose of OB, however, progesterone induced an LH release with two peaks in all animals. The peak latency (7·3 ±0·9 h) and the duration (19·3 ±1·3 h) of the first response with 30 μg OB + progesterone were virtually identical to those with 10 μg OB + progesterone (7·0 ±0·7 h, 18·0 ± 1·4 h respectively), whilst both components of the first response with 30 μg OB + progesterone were significantly shorter than those with 30 μg OB + oil (P < 0·001 for both). The peak latency of the second response with 30 μg OB + progesterone (42·7+ 4·8 h) was similar to that with 10 μg OB + progesterone (38·3 ±3·2 h), but the duration of the second response with 30 μg OB + progesterone (46·0 ± 1·7 h) was longer than that (35·7 ±3·2 h) with 10 μg OB + progesterone (P <0·02). In the second series of experiments the same nine animals received an OE2-capsule implantation and 10 μg OB (subthreshold) injections before pentobarbitone and progesterone. Pentobarbitone was first given 6 h before progesterone and additional injections were made to maintain the anaesthetized state for 21·6 ± 1·3 h. This period was to cover the progesterone-induced first LH response. Pentobarbitone completely blocked the expected first response of the progesterone-induced LH release in six animals. In the remaining three animals an enhanced LH surge occurred, but it consisted of a single peak with long latency 16·0 ± 2·0 h) and duration (66·0 ± 10·5 h) and was essentially the same as that observed in animals treated with a suprathreshold dose (30 μg) of OB alone. Anaesthesia did not, on the other hand, alter the response of the pituitary gland to LH releasing hormone. Therefore it was concluded that (1) sequential administration of oestrogen and progesterone induces an LH release with two phases in the ovariectomized monkey and (2) the facilitatory action of progesterone on the first phase of LH release requires the involvement of the brain.


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