Effects of tamoxifen on concentrations of luteinizing hormone and follicle-stimulating hormone in the plasma of ovariectomized ewes

1983 ◽  
Vol 99 (1) ◽  
pp. 23-29 ◽  
Author(s):  
I. J. Clarke
Keyword(s):  
Plasma Concentrations ◽  
Tamoxifen Treatment ◽  
Similar Response ◽  
Lh Surge ◽  
Peripheral Plasma ◽  
Mediated Effects ◽  
Tamoxifen Citrate ◽  
Oestradiol Benzoate ◽  
Antagonist Action ◽  
Lh Secretion

The effects of tamoxifen on peripheral plasma concentrations of gonadotrophins were studied in ovariectomized ewes. First, ovariectomized ewes were injected (i.m.) with 10 mg tamoxifen citrate/day for 4 days which caused a significant reduction in plasma LH concentrations within 4 days and plasma FSH concentrations within 1 day of the commencement of treatment. Further groups of ovariectomized ewes were then injected (i.m.) with two injections of 10 mg tamoxifen citrate 6 h apart or 20 μg oestradiol benzoate (OB) or tamoxifen citrate plus OB or oil. Tamoxifen treatment caused a reduction in plasma LH and FSH concentrations within 6 h. In four of our ewes receiving OB, a surge in LH secretion was observed; a similar response was observed in two out of four ewes given the combination of tamoxifen citrate and OB. No LH surge was seen in ovariectomized ewes given tamoxifen alone. These results show that tamoxifen reduces plasma gonadotrophin levels in ovariectomized ewes suggesting it is an oestrogen agonist in the sheep pituitary gland. A partial oestrogen antagonist action of tamoxifen is similarly suggested by its ability to block the oestrogen-induced LH surge in some ovariectomized ewes. Since tamoxifen consistently lowers plasma gonadotrophin levels in ovariectomized ewes this could result from action via oestrogen receptors or by central nervous system, non-oestrogen receptor-mediated effects.

Differential responses of hypothalamic LHRH-I and -II to castration and gonadal steroid or tamoxifen treatment in cockerels

1990 ◽  
Vol 125 (1) ◽  
pp. 139-146 ◽  
Author(s):  
S. C. Wilson ◽  
R. T. Gladwell ◽  
F. J. Cunningham
Keyword(s):  
Plasma Concentration ◽  
Testosterone Propionate ◽  
Plasma Concentrations ◽  
Suppressive Effect ◽  
Posterior Hypothalamus ◽  
Gonadal Steroids ◽  
Tamoxifen Treatment ◽  
Gonadal Steroid ◽  
Oestradiol Benzoate ◽  
Lh Secretion

ABSTRACT Changes in the hypothalamic contents of LHRH-I and LHRH-II were determined in intact and castrated cockerels injected i.m. with gonadal steroids or tamoxifen. An increase in the plasma concentration of LH after castration was accompanied by a significant increase in the content of LHRH-I in the posterior hypothalamus (including the mediobasal hypothalamus and median eminence) which was reversed by oestradiol benzoate given on days 14 and 15 after castration. Under similar circumstances, testosterone propionate did not modify the hypothalamic content of LHRH-I, even though both steroids reduced the plasma concentrations of LH to levels below those of intact cockerels. Treatment of intact cockerels with oestradiol benzoate significantly increased the content of LHRH-I in the posterior hypothalamus, whilst testosterone propionate was again without effect. Tamoxifen significantly raised the plasma concentration of LH in intact cockerels and partially antagonized the suppressive effect of oestradiol benzoate and testosterone on LH secretion in castrated cockerels. However, an anti-oestrogenic effect of tamoxifen on the hypothalamic content of LHRH-I was not demonstrated. There was no evidence of any changes in the hypothalamic content of LHRH-II after castration, with or without gonadal steroid replacement. A change in the hypothalamic content of LHRH-I in response to manipulation of the steroid environment would imply an involvement of this peptide in the mechanism by which gonadal steroids regulate the release of LH. The absence of changes in the hypothalamic content of LHRH-II in the same circumstances suggest that it is not directly involved in the control of LH secretion by the gonadal steroid negative feedback loop. Journal of Endocrinology (1990) 125, 139–146

Pulsatile administration of gonadotrophin-releasing hormone stimulates, in oestrogen-treated anaesthetized ovariectomized ewes, a surge release of LH qualitatively and quantitatively different from that induced by oestradiol in conscious ovariectomized ewes

1988 ◽  
Vol 116 (1) ◽  
pp. 143-148 ◽  
Author(s):  
P. J. Wright ◽  
I. J. Clarke
Keyword(s):  
Plasma Concentrations ◽  
Lh Surge ◽  
Releasing Hormone ◽  
Treatment Regimens ◽  
Oestradiol Benzoate ◽  
Pulsatile Administration ◽  
Gonadotrophin Releasing Hormone ◽  
Induction Of Anaesthesia ◽  
Lh Secretion ◽  
Conscious Control

ABSTRACT The nature of the gonadotrophin-releasing hormone (GnRH) stimulus of the pituitary necessary for the oestrogen-induced plasma LH surge was studied in ovariectomized ewes. The sheep were treated with oestradiol benzoate (50 μg i.m.) at 0 h, and the hypothalamic contribution to the LH surge was blocked by pentobarbitone anaesthesia over the time during which the surge was expected (11–31 h). Pituitary responsiveness to exogenous GnRH (100 ng) administered i.v. in a pulsatile mode (once per hour or once per 20 min) over the period 15–30 h was assessed from plasma concentrations of LH. Neither of the GnRH treatments induced patterns of LH secretion similar to those seen in conscious ovariectomized ewes given oestrogen only. Plasma LH secretion in response to hourly GnRH pulses was less (P<0·01) than that associated with oestrogen-induced plasma LH surges in conscious control ewes. With pulses of GnRH administered every 20 min the amount of LH released was greater (P<0·05) than that in oestrogen-treated conscious control ewes. In contrast to the single surge induced by oestradiol in conscious ewes, GnRH pulses given every 20 min elicited phasic patterns of LH secretion consisting of two or three distinct surges. The failure of GnRH treatment to elicit an LH surge similar to an oestrogen-induced surge could reflect inappropriate GnRH treatment regimens, and/or inadequate priming of the pituitary with GnRH after induction of anaesthesia but before GnRH treatment. J. Endocr. (1988) 116, 143–148

Dissociation between the ovarian factors controlling sexual receptivity and preovulatory secretion of LH in cyclic female rats

1987 ◽  
Vol 112 (1) ◽  
pp. 133-138 ◽  
Author(s):  
P. Södersten ◽  
P. Eneroth
Keyword(s):  
Sexual Behaviour ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Sexual Receptivity ◽  
Serum Progesterone ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion ◽  
Intact Rats

ABSTRACT Ovariectomy and treatment with oestradiol benzoate (10 μg OB) on the day before behavioural oestrus eliminated the preovulatory surge of LH and reduced the level of sexual receptivity on the following day. Sexual behaviour, but not the LH surge, was restored by progesterone (0·5 mg) given 18 h later. Injection of OB on the day after behavioural oestrus induced a small release of LH and normal sexual behaviour on the following day. Ovariectomy on the day after behavioural oestrus reduced the stimulatory effect of OB on sexual behaviour and eliminated its weakly stimulatory effect on LH release. Sexual behaviour, but not the small LH surge, was restored in these animals by progesterone (0·5 mg) given 18 h later. Treatment of rats ovariectomized 2 days before the day of the LH surge with implants containing oestradiol or injections of oestradiol (1 μg) induced LH surges but the amplitudes of these LH surges were much smaller than those of the normal LH surge. Treatment of intact rats with OB increased serum progesterone levels 24 h later, an effect which was eliminated by ovariectomy. Injections of LH (20 μg) into intact rats on the day after behavioural oestrus also increased serum progesterone concentrations but failed to stimulate sexual behaviour. It is suggested that OB treatment of intact rats on the day after behavioural oestrus stimulates sexual behaviour by inducing a surge of LH secretion which activates ovarian secretion of progesterone. Thus, oestrogen and progesterone but not the LH surge are essential for sexual behaviour. Whereas oestradiol and progesterone restore normal sexual behaviour in ovariectomized rats, additional ovarian factors may be required for induction of normal LH surges. J. Endocr. (1987) 112, 133–138

Mechanisms responsible for suppression of FSH and LH during lactation in the rat

1991 ◽  
Vol 129 (1) ◽  
pp. 119-130 ◽  
Author(s):  
K. Taya ◽  
S. Sasamoto
Keyword(s):  
Plasma Concentrations ◽  
The Other ◽  
Primary Role ◽  
Ovarian Steroids ◽  
Unilateral Ovariectomy ◽  
Peripheral Plasma ◽  
The Mean ◽  
Lh Secretion ◽  
Ovarian Inhibin ◽  
Venous Plasma

ABSTRACT Mechanisms responsible for suppression of FSH and LH secretion during lactation were investigated in rats, with special reference to the suckling stimulus and ovarian inhibin. Concentrations of immunoreactive inhibin in the peripheral plasma and bioactive inhibin in ovarian venous plasma were always low on days 3 and 5 of lactation in dams nursing eight pups, whereas values were always high on days 17 and 20 of lactation in dams nursing eight pups and on day 5 of lactation in dams nursing two pups. There was an FSH surge within 48 h after removal of litters on days 3 and 5 of lactation in dams nursing eight pups, whereas plasma concentrations of FSH were unchanged within 48 h by removal of litters on days 17 and 20 of lactation in dams nursing eight pups and on day 5 of lactation in dams nursing two pups. Plasma LH concentrations increased significantly compared with those of control animals within 24 h after removal of the litter on any day of lactation, regardless of the litter size. Plasma FSH levels increased within 6 h after bilateral or unilateral ovariectomy in lactating rats only on the days when plasma concentrations of inhibin were high before ovariectomy, such as day 17 of lactation in dams nursing eight pups and on day 5 of lactation in dams nursing two pups, whereas the mean concentrations of plasma LH showed no significant increase within 12 h after bilateral ovariectomy in these lactating rats. Treatment with progesterone or oestradiol-17β after unilateral ovariectomy did not inhibit the increase in plasma FSH levels, while the increase in plasma concentrations of FSH after surgery was completely inhibited by injecting inhibin (porcine follicular fluid). Treatment with steroid hormones inhibited the basal levels of LH in unilateral ovariectomized lactating rats. Plasma FSH concentrations increased sharply within 6 h after a single i.v. injection of anti-inhibin serum on days 10, 15 and 20 of lactation in dams nursing eight pups and on day 5 of lactation in dams nursing two pups, whereas only a small but significant increase in concentrations of FSH was noted 6 h after the antiserum treatment on day 5 of lactation in dams nursing eight pups. Concentrations of plasma LH were unchanged by treatment with antiserum in lactating rats throughout lactation. These findings indicate that the suckling stimulus, rather than ovarian factors, is mainly responsible for the suppression of FSH as well as LH secretion during the first half of lactation in rats nursing eight pups. On the other hand, during the second half of lactation in rats nursing eight pups and throughout lactation in rats nursing two pups, ovarian inhibin plays a primary role in the suppression of FSH secretion, whereas ovarian steroids act to suppress LH secretion. Journal of Endocrinology (1991) 129, 119–130

Suppression of LH response to gonadotrophin-releasing hormone or oestradiol by ACTH(1–24) treatment in anoestrous ewes

1988 ◽  
Vol 118 (2) ◽  
pp. 193-197 ◽  
Author(s):  
H. Dobson ◽  
S. A. Essawy ◽  
M. G. S. Alam
Keyword(s):  
Plasma Concentrations ◽  
Suppressive Effect ◽  
Reproductive Efficiency ◽  
Adrenocorticotrophic Hormone ◽  
Releasing Hormone ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Gonadotrophin Releasing Hormone ◽  
Baseline Values ◽  
Lh Secretion

ABSTRACT Stress is known to result in lowered female reproductive efficiency. The objective of this study was to examine how increased pituitary-adrenal activity may influence gonadotrophin release in anoestrous ewes. Various doses (0·06–1·0 mg) of a synthetic adrenocorticotrophic hormone (ACTH(1–24)) preparation were injected into ewes 30 min or 3 h before an i.v. injection of 500 ng gonadotrophin-releasing hormone (GnRH). The LH response to GnRH given 30 min after ACTH(1–24) was similar to that after GnRH alone, whereas the response 3 h after ACTH(1–24) was significantly lower, irrespective of the dose of ACTH(1–24). At 30 min and 3 h after ACTH(1–24) the concentrations of cortisol exceeded 50 nmol/l compared with baseline values of < 10 nmol/l. The effect of ACTH(1–24) on oestradiol-induced LH release was also examined. Those ewes receiving 0·8 mg ACTH(1–24) depot and 50 μg oestradiol benzoate simultaneously had a preovulatory-type increase in LH 14–20 h later, similar to when oestradiol benzoate was given alone. None of the ewes receiving an additional 0·8 mg ACTH(1–24) depot 10 h after oestradiol benzoate had increases in LH concentration. The cortisol concentrations in all ewes receiving either one or two injections of ACTH(1–24) were > 35 nmol/l at 10 h after the oestradiol injection. However, concentrations of progesterone increased from 0·9 ± 0·3 (s.e.m.) nmol/l at the time of the second ACTH(1–24) injection to 2·1 ±0·3 nmol/l after 2 h. In summary, it would appear that the suppressive effect of ACTH(1–24) on LH secretion induced by GnRH or oestradiol in the anoestrous ewe is not dependent on increased plasma concentrations of cortisol. J. Endocr. (1988) 118, 193–197

Vasoactive intestinal peptide inhibits the steroid-induced LH surge in the ovariectomized rat

1992 ◽  
Vol 133 (3) ◽  
pp. 433-437 ◽  
Author(s):  
R. F. Weick ◽  
K. M. Stobie
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Critical Period ◽  
Control Sample ◽  
Ovariectomized Rats ◽  
Lh Surge ◽  
The Third ◽  
Oestradiol Benzoate ◽  
Short Time ◽  
Lh Secretion ◽  
Secretion Rates

ABSTRACT The LH surge was induced in ovariectomized rats by sequential treatment with oestradiol benzoate and progesterone. Vasoactive intestinal peptide (VIP) or saline was infused into the third cerebral ventricle from 13.30 to 16.30 h on the afternoon of the anticipated LH surge. Two blood samples were taken by jugular puncture from each animal, one at 12.00 h as a control sample and the other at 16.00, 18.00, 20.00 or 22.00 h. Saline-infused animals showed a normal LH surge, with mean plasma LH concentrations reaching a peak at 18.00 h, declining by 20.00 h and reaching control (12.00 h) levels by 22.00 h. Plasma LH in animals infused with VIP was not significantly higher than control levels at 16.00 or 18.00 h. By 20.00 h, mean LH levels in VIP-infused rats had risen to the levels seen at that time in saline-infused rats, and by 22.00 h LH had returned to control levels in VIP-infused animals. We interpret these findings to mean that VIP inhibits LH secretion during the LH surge. It does not block the surge completely, as pentobarbital during the critical period would have done; nor does VIP appear to affect the timing of the LH surge. Rather, VIP inhibits the increased LH secretion rates of the LH surge only during the period of VIP treatment and for a short time afterward. Journal of Endocrinology (1992) 133, 433–437

Anaesthesia with alphaxalone plus alphadolone acetate blocks the oestrogen-stimulated LH surge and impairs pulsatile LH secretion in ovariectomized female rats

1984 ◽  
Vol 102 (1) ◽  
pp. 27-31 ◽  
Author(s):  
R. G. Dyer ◽  
S. Mansfield
Keyword(s):  
Body Weight ◽  
Female Rats ◽  
Lh Surge ◽  
Group Of Seven ◽  
Oestradiol Benzoate ◽  
Anaesthetized Rats ◽  
Lh Secretion

ABSTRACT Two experiments were undertaken to assess further the action of the steroid anaesthetic alphaxalone upon LH secretion in chronically ovariectomized female rats. For the first experiment, 31 rats were given two injections of oestradiol benzoate (20 μg/100 g body weight), each 72 h apart, to stimulate an LH surge 6 h after the second injection. However, one group of seven rats was anaesthetized with alphaxalone throughout the 6-h period and a second group of eight was similarly anaesthetized only for the last 2 h of the 6-h period. The steroid-stimulated LH surge was blocked in both groups of rats anaesthetized with alphaxalone. The second experiment involved a comparison of pulsatile LH secretion in animals which were either unanaesthetized (n = 8) or anaesthetized with alphaxalone (n = 9). In six out of nine rats the anaesthetic did not affect the maximum or minimum plasma LH concentrations but significantly slowed the frequency at which LH pulses were measured. In the remaining three anaesthetized rats the drug blocked pulsatile LH secretion. The experiments confirm that some secretion of LH continues during alphaxalone anaesthesia but indicate also that the drug has a more deleterious action upon the oestrogen-stimulated LH surge than believed hitherto. J. Endocr. (1984) 102, 27-31

Evidence for the involvement of central conversion of testosterone to oestradiol-17β in the regulation of luteinizing hormone secretion in the cockerel

1983 ◽  
Vol 99 (2) ◽  
pp. 301-310 ◽  
Author(s):  
S. C. Wilson ◽  
P. G. Knight ◽  
F. J. Cunningham
Keyword(s):  
Testosterone Propionate ◽  
Hormone Secretion ◽  
Plasma Concentrations ◽  
Passive Immunization ◽  
Inhibitory Influence ◽  
Luteinizing Hormone Secretion ◽  
Depressive Effect ◽  
Oestradiol Benzoate ◽  
Lh Releasing Hormone ◽  
Lh Secretion

Treatment of intact cockerels with the synthetic antioestrogen tamoxifen caused a significant increase in the plasma concentration of LH. In contrast, passive immunization with an antiserum raised against oestradiol-17β did not lead to an increase in plasma LH. A pronounced depressive effect of injections of 0·1 mg testosterone propionate (TP) or 0·1 mg oestradiol benzoate (OB) on plasma concentrations of LH was prevented by tamoxifen. Furthermore, a pronounced rise in the concentration of LH releasing hormone in the posterior hypothalamus after the injection of cockerels with OB was completely inhibited by tamoxifen. Neither 0·1 nor 0·5 mg androstenedione modified the concentration of LH in plasma. A dose of 0·05 mg TP, which failed to depress the concentration of LH in plasma of intact cockerels, caused a marked fall in plasma LH in castrated cockerels. Tamoxifen itself exhibited weak oestrogen agonist activity in castrated cockerels by causing a reduction in the concentration of LH in plasma. However, tamoxifen prevented any further depressive effect on LH resulting from the injection of TP. These findings suggest that testosterone exerts an inhibitory influence on LH secretion at the central neural level, partially at least, by means of the product of its aromatization, oestradiol-17β.

Analysis of the ratio of biological to immunological LH secreted during the oestrogen-induced LH surge in the ewe

1990 ◽  
Vol 127 (2) ◽  
pp. 217-222 ◽  
Author(s):  
I. J. Clarke ◽  
L. M. Foulds ◽  
S. Hayward ◽  
J. T. Cummins ◽  
D. M. Robertson
Keyword(s):  
Plasma Concentrations ◽  
Serum Samples ◽  
Lh Surge ◽  
Oestradiol Benzoate ◽  
Unknown Composition ◽  
Radio Immunoassay ◽  
Pass Through ◽  
Highly Correlated ◽  
The Relationship

ABSTRACT Plasma concentrations of in-vitro biological and immunological LH were measured throughout the LH surge in cyclic ewes and in ovariectomized ewes treated i.m. with oestradiol benzoate. Both activities increased in parallel during the LH surge in both groups, although the ratio of biological to immunological activities (B/I ratio) was highest at the peak of the LH surge. The two activities were highly correlated (r = 0·86–0·92), with similar slopes from their regression analysis for the cyclic and ovariectomized groups (1·15 and 1·16 respectively). However, the intercepts of the regression lines did not pass through the origin, but intersected the y (radio-immunoassay) axis, suggesting that these serum samples contained immunoactivity not associated with LH bioactivity. In conclusion, an increase in the LH B/I ratio was observed during the LH surge in oestrogen-treated ovariectomized ewes and in cyclic ewes. This increase was not attributable to a change in the relationship between these two LH activities during the LH surge, but rather to the detection of bioinactive immunoactive material in plasma of unknown composition. Journal of Endocrinology (1990) 127, 217–222

Blockade of pro-oestrus LH surge and ovulation by GABA increase in the rat locus coeruleus

1987 ◽  
Vol 115 (4) ◽  
pp. 490-496 ◽  
Author(s):  
Adriana I. Landa ◽  
Alfredo O. Donoso
Keyword(s):  
Locus Coeruleus ◽  
Plasma Concentrations ◽  
Aminobutyric Acid ◽  
Plasma Prolactin ◽  
Gamma Aminobutyric Acid ◽  
Gaba Transaminase ◽  
Lh Surge ◽  
Lh Release ◽  
Lh Secretion ◽  
Gaba Transaminase Inhibitor

Abstract. The effects of gamma-aminobutyric acid (GABA) increase at the nucleus locus coeruleus (LC) on pro-oestrus LH release and ovulation were evaluated in rats. Local microinjection of the GABA-transaminase inhibitor gamma-vinyl-GABA (GVG) produced 6 h later a marked increase in GABA in the LC. Such action caused a significant decrease of plasma LH levels and prevented the pro-oestrus LH surge. In some animals, plasma prolactin levels were also lowered, but in others its plasma concentrations were high and similar to that in controls. Ovulation did not occur in the rats treated with GVG. In additional experiments, the periventricular gray substance (PGS) close to the locus coeruleus was injected with GVG. Results obtained show a LH surge blockade and failure of ovulation in most of these rats. These findings may be interpreted on the basis of GABA action on rostral LC cells that project to the PGS. The results altogether suggest that through neurons of the locus coeruleus, GABA may exert an inhibitory role in the regulation of LH secretion.

Sign in / Sign up

Export Citation Format

Share Document