bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of the progesterone antagonist mifepristone on the hypothalamo-hypophysial-ovarian axis in rats
Authors: van der Schoot P. , Uilenbroek J. Th. J. , Slappendel E. J. 
Published: December 2008

ABSTRACT
Treatment of female rats for 3 weeks with the antigestagen 1 1β-(4-dimethylaminophenyl)-17β-hydroxy-17α-(prop-1 -ynyl)-estra-4,9-dien-3-one (mifepristone) results in pituitary and ovarian enlargement. The present study dealt with the possible mechanism(s) of these responses.
Ovarian enlargement appeared to be dependent upon prolactin. In the absence of prolactin, during combined treatment with mifepristone and the dopamine agonist 2-Br-α-ergokryptine, ovarian growth was significantly suppressed. It was unclear why persistent hyperprolactinaemia, due to treatment with mifepristone, resulted in persistence of functionally active corpora lutea despite intermittent ovulation, while persistent hyperprolactinaemia due to ectopic pituitary grafts did not.
Pituitary enlargement appeared to be dependent upon the persistence of ovarian oestrogen secretion during the treatment period. Ovariectomy or lactation fully inhibited this response. Pituitary enlargement and prolactin secretion in ovariectomized rats in response to exogenous oestrogen (injections of oestradiol benzoate) were significantly enhanced by additional treatment with mifepristone. It is concluded that mifepristone facilitates the effect of oestrogen on pituitary lactotrophs, thereby enhancing pituitary growth.
Ovarian enlargement during treatment with mifepristone may be specific for rats due to the luteotrophic action of prolactin in these animals. Pituitary enlargement due to facilitation of oestrogen-induced pituitary growth may become a focus of attention when this or similar antigestagenic drugs are being used for prolonged periods in clinical trials, e.g. for limiting steroid-sensitive tumour growth.
Journal of Endocrinology (1990) 124, 425–432
Characterization of α1-adrenergic receptor subtypes linked to iodide efflux in rat FRTL cells
Authors: Shimura H. , Endo T. , Tsujimoto G. , Watanabe K. , Hashimoto K. , Onaya T. 
Published: December 2008

ABSTRACT
We have characterized α1-adrenergic receptor subtypes in functional rat thyroid cells, FRTL, with relation to iodide efflux, and have also examined the effect of TSH on α1 receptor subtypes. FRTL cells grown in a medium containing 5 mU TSH/ml (6H cells) had five times the number of α1 receptors of those maintained in TSH-free medium (5H cells) (11·2 fmol/106 cells compared with 2·0 fmol/106 cells). Pretreatment with chlorethylclonidine (CEC; 10 μmol/l), which inactivates only α1b receptors, caused 98·8% and 97·0% decreases in the density of specific [3H]prazosin-binding sites in 5H and 6H cells respectively. LIGAND computer program analysis of the displacement curves for 2-(2,6-dimethoxyphenoxyethyl)-aminomethyl-1,4 benzodioxane (WB4101) showed that FRTL cells contained mostly low-affinity WB4101 sites. Using the phenoxybenzamine inactivation method, we found a linear relationship between α1 receptor density and the cytosolic free Ca2+ concentration response in FRTL cells. Pre-exposure of intact FRTL cells to CEC caused a 98·7% decrease in noradrenaline-stimulated maximal increase in cytosolic free Ca2+. Also, CEC and 3,4,5-trimethoxybenzoic acid 8-(diethylamino) octyl ester (TMB-8), but not nicardipine, inhibited noradrenaline-stimulated iodine efflux. The results suggest that FRTL cells contain mostly the α1b-adrenergic receptor subtype; that the α1b receptors mediate cytosolic free Ca2+ and iodide efflux responses, and that TSH enhances these responses by increasing the α1b receptor density without affecting the post-receptor mechanism.
Journal of Endocrinology (1990) 124, 433–441
Production of anti-idiotypic antisera to rat GH antibodies capable of binding to GH receptors and increasing body weight gain in hypophysectomized rats
Authors: Gardner M. J. , Morrison C. A. , Stevenson L. Q. , Flint D. J. 
Published: December 2008

ABSTRACT
Anti-idiotypic antibodies to rat GH antibodies were produced in both sheep and mice and shown to be capable of mimicking GH by inhibiting 125I-labelled ovine GH (oGH) binding to sheep liver membranes. The sheep anti-idiotypes were characterized further and shown to (1) inhibit 125I-labelled oGH binding to oGH antibodies, (2) inhibit 125I-labelled oGH binding to rat adipocytes and (3) be incapable of inhibiting the binding of either 125I-labelled ovine prolactin or 125I-labelled bovine insulin to sheep liver membranes. This indicated that the antibodies were not limited to certain species or tissues, but were hormone specific. Finally, these anti-idiotypic antibodies were also capable of stimulating an increase in body weight gain in hypophysectomized rats, suggesting that they may be functional as well as structural mimics of GH, although the increased body weight gain was not accompanied by any increase in circulating concentrations of insulin-like growth factor-I.
Journal of Endocrinology (1990) 125, 53–59
Regulation by GH of insulin-like growth factor-I mRNA expression in rat epiphyseal growth plate as studied with in-situ hybridization
Authors: Nilsson A. , Carlsson B. , Isgaard J. , Isaksson O. G. P. , Rymo L. 
Published: December 2008

ABSTRACT
Expression of insulin-like growth factor I (IGF-I) mRNA and its dependence on GH was studied in rat epiphyseal growth plate by in-situ hybridization. Methodological aspects of the technique were first evaluated on fixed sagittal cryosections from 28-day-old rat epiphyseal growth plates to ascertain specific hybridization. In-situ hybridization was compared on sections from 10- and 28-day-old rats and the GH-dependence was studied in 35-day-old hypophysectomized rats. Expression of IGF-I mRNA was apparent in chondrocytes of the proliferative, hypertrophic and early degenerative zones of the growth plate of 28-day-old rats. The epiphyseal growth plate from 10-day-old rats showed a weak hybridization signal compared with 28-day-old rats. In contrast, the mesenchymal cells of the periosteum of 10-day-old rats showed a rather strong hybridization signal. Hypophysectomy resulted in a reduction in hybridization signal and cell number of the growth plate compared with 35-day-old age-matched normal rats. GH-Replacement therapy (200 μg human GH s.c. every 4 h for 24 h) resulted in partially restored expression of IGF-I mRNA.
The present study has shown that the IGF-I gene is expressed in the rat epiphyseal growth plate chondrocytes and that the expression is dependent on GH. The results support a paracrine/autocrine role of IGF-I for the expression of the stimulatory effect of GH on longitudinal bone growth.
Journal of Endocrinology (1990) 125, 67–74
Possible site of action of 5-hydroperoxyeicosatetraenoic acid derived from arachidonic acid in ACTH-stimulated steroidogenesis in rat adrenal glands
Authors: Mikami K. , Omura M. , Tamura Y. , Yoshida S. 
Published: December 2008

ABSTRACT
The site of action of 5-hydroperoxyeicosatetraenoic acid (5-HPETE) in ACTH-induced stimulation of steroidogenesis was examined in rat adrenocortical fasciculata cells. Prior addition of AA861, a specific inhibitor of 5-lipoxygenase, had no significant effect on cyclic AMP-dependent protein kinase activity and cholesterol esterase activities, when stimulated by ACTH in adrenocortical cells, compared with that stimulated by ACTH alone. Cholesterol accumulation in the mitochondria of cells treated with ACTH and cycloheximide was also not altered by pretreatment with AA861. We found, however, that pregnenolone formation, stimulated by ACTH, decreased in a dose-dependent manner when cells were pretreated with AA861. The inhibition of ACTH-stimulated pregnenolone formation by treatment with AA861 was restored only by prior addition of 5-HPETE. Furthermore, addition of AA861 also did not affect the conversion of pregnenolone into corticosterone.
In conclusion, 5-HPETE may act at the level of the mitochondria in ACTH-induced steroidogenesis in rat adrenal fasciculata cells.
Journal of Endocrinology (1990) 125, 89–96
Differential responses of hypothalamic LHRH-I and -II to castration and gonadal steroid or tamoxifen treatment in cockerels
Authors: Wilson S. C. , Gladwell R. T. , Cunningham F. J. 
Published: December 2008

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
Steroid, corticotrophin-releasing hormone, ACTH and prostaglandin interactions in the amnion and placenta of early pregnancy in man
Authors: Jones S. A. , Challis J. R. G. 
Published: December 2008

ABSTRACT
Corticotrophin-releasing hormone (CRH) is produced by both the placenta and fetal membranes at term in man, and CRH mRNA has been detected in human placental tissue. The synthesis of CRH and its control during early pregnancy, however, have not been established, and the role of CRH produced in the placenta and fetal membranes is not known.
We examined whether amnion and placental tissue obtained between 12 and 15 weeks of gestation produced CRH in vitro, whether steroid modulation of output occurred and whether CRH affected prostaglandin (PG) output by the placenta and amnion.
Immunoreactive (ir) CRH output by amnion (2·8 ± 0·31 (s.e.m.) nmol/105 cells) was significantly (P<0·01) greater than that from placenta (1·76 ± 0·21 nmol/105 cells). Output of ir-CRH decreased in the presence of progesterone, but increased in the presence of cortisol and dexamethasone. There was no significant effect of progesterone or ir-CRH output by placental cells; however, ir-CRH output was increased in the presence of dexamethasone and cortisol. There was no significant effect of corticosterone on ir-CRH output by either amnion or placental cells. Both ACTH and CRH stimulated the output of PGE2 and PGF2α by amnion cells. In contrast, there was no significant effect of PGE2 output by placental cells maintained in the presence of either human CRH or ACTH. Output of PGF2α by placental cells was increased in the presence of both CRH and ACTH.
We conclude that both amnion and placental tissue produce CRH in early gestation, and that this output is modulated by steroids. CRH and ACTH stimulate PG output by amnion and placenta in early pregnancy, raising the possibility of local (autocrine and paracrine) interrelations in vivo.
Journal of Endocrinology (1990) 125, 153–159
Influence of chronic oestrogen treatment on the density of muscarinic cholinergic receptors and calcium channels in the rabbit uterus
Authors: Batra S. 
Published: December 2008

ABSTRACT
Ovariectomized rabbits were treated for 1 or 8 weeks with oestrogen and the effects on uterine weight, muscarinic receptor density and nitrendipine-binding sites on myometrial membranes were studied. The wet weight of the uterus after 1 week of oestrogen treatment increased more than tenfold and increased further by approximately 50% after 8 weeks of oestrogen treatment. The muscarinic receptor density increased significantly after 1 week of oestrogen treatment. Although there was no further increase in receptor density with continuing oestrogen treatment up to 8 weeks, the muscarinic receptor affinity increased significantly. The density of nitrendipine-binding sites increased sixfold after 1 week of oestrogen treatment and did not change thereafter. Oestrogen treatment had no influence on the affinity of nitrendipine-binding sites. The increase by oestrogen in muscarinic receptor density and in nitrendipine-binding sites as shown by the present data is consistent with the generally reported increase in agonist-induced contractile response of the myometrium following oestrogen treatment.
Journal of Endocrinology (1990) 125, 185–189
The cytochrome P45017α (17α-hydroxylase/C17,20-lyase) activity of the junctional zone of the rat placenta
Authors: Johnson D. C. , Sen M. 
Published: December 2008

ABSTRACT
The cytochrome P450 responsible for androgen synthesis by the placenta during the second half of pregnancy in the rat was studied in intact and hypophysectomized animals. The two activities of P45017α, 17α-hydroxylase and C17,20-lyase, were limited to the junctional zone.
C17,20-Lyase activity was greater with progesterone than with 17-hydroxyprogesterone as substrate. Although the apparent Michaelis constants were similar, progesterone had a higher maximum velocity than 17-hydroxyprogesterone. Regardless of substrate, C17,20-lyase activity was greater with NADPH than with NADH as an electron donor, and there was no additive effect using both cofactors.
Administration of human chorionic gonadotrophin (hCG; 10IU at 09.00 and 21.00 h on days 13 and 14 and at 09.00 h on day 15) to intact females resulted in more than a 50% reduction of enzyme activity when measured on day 15. The same dose of hCG given to hypophysectomized animals with delayed implantation, i.e. pituitary removal on day 3 and implantation induced by oestrone 5 days later, had no effect on placental enzyme activity, but increased that in the ovary. Administration of ovine LH by osmotic minipump (days 11–15) to intact females resulted in abortion in all animals. The same treatment to animals hypophysectomized on day 11 produced abortion in three of four rats; enzyme activity was greatly reduced in the single animal with placentas. In contrast, infusion of LH into hypophysectomized animals with delayed implantation increased placental enzyme activities. However, administration of 20IU pregnant mare's serum gonadotrophin to the hypophysectomized animals on day 11 produced a large increase in ovarian follicular development and ovarian P45017α activities, and resulted in abortion in three of five animals within 96 h.
The results indicate that the P45017α of the junctional zone of the rat placenta has characteristics similar, if not identical, to those of the ovary with regard to preference of substrate and electron donor. However the enzyme activity in the placenta did not increase to the same extent as that in the ovary when exposed to gonadotrophins with LH activity, suggesting that the control mechanisms may be different.
Journal of Endocrinology (1990) 125, 217–224
Available FSH receptors in adult rat testis in vivo
Authors: Yoon D. J. , Reggiardo D. , David R. 
Published: December 2008

ABSTRACT
It has been suggested that the tight junctions formed between Sertoli cells during the peripubertal period constitute a barrier to circulating FSH in the adult testis, limiting its access to the lumen of the seminiferous tubules. There are also reports of FSH receptor-binding inhibitors. These obervations prompted us to study the extent of FSH receptor availability in vivo in the adult rat. Experimental rats were given an intracardiac injection of rat FSH (rFSH), and the occupied receptor was measured by radioimmunoassay of acid-released rFSH from the testis. In the saline-injected control animals, there were 247 fmol occupied FSH receptors/g testis, and as much as 1788 fmol of the unoccupied high-affinity receptors/g testis, as measured by in-vitro binding studies. After intracardiac injection of increasing amounts of rFSH (up to 606 pmol), receptor occupancy increased to a maximum plateau of only 448 fmol/g testis. In contrast, when rFSH was given by intratesticular injection in order to achieve pharmacological doses in the testis, the maximum binding was 662 fmol/g testis. Scatchard analysis of the in-vivo data revealed, however, that the maximum concentration of the high-affinity receptor was 452 fmol/g testis, a value concordant with the highest in-vivo binding observed in animals given intracardiac rFSH (448 fmol/g). A single injection of the hormone did not induce down-regulation of FSH receptors, regardless of the dose, whereas multiple injections of menotrophin were effective, at least to some extent. Despite the receptor loss, the immediate receptor availability was maintained, suggesting the presence of a receptor pool.
In conclusion, in-vivo binding of FSH to its high-affinity receptor is limited in adult rat testis, and the available receptor concentration appears to be regulated so as to maintain a constant level.
Journal of Endocrinology (1990) 125, 293–299
Enzyme-linked immunosorbent assay for human insulin-like growth factor-I using monoclonal and polyclonal antibodies with defined epitope recognition
Authors: Tamura K. , Kobayashi M. , Suzuki S. , Ishii Y. , Koyama S. , Yamada H. , Hashimoto K. , Niwa M. , Shibayama F. 
Published: December 2008

ABSTRACT
Monoclonal antibodies (McAb) and polyclonal antibodies (PcAb) against human insulin-like growth factor-I (somatomedin C; hIGF-I) were produced. Using these two antibodies, an enzyme-linked immunosorbent assay (ELISA) system for hIGF-I was established. The ELISA system was able to detect hIGF-I at a range of 1–25 μg/l, compared with the range of 1–50 μg/l detected by radioimmunoassay (RIA). Human IGF-II and human insulin could not be recognized in this system. The plasma concentrations of IGF-I found using the ELISA agreed well with those found using RIA after conventional Sep-Pak C18 cartridge pretreatment. Epitopes of hIGF-I to McAb and PcAb were investigated by enzymatic digestion of hIGF-I followed by comparing the affinity of the antibodies to the peptides obtained proteolytically. The epitope to McAb was found to be a peptide containing Leu10-Val11-Asp12 (epitope 2). Five epitopes to PcAb containing the following key fragments were identified: a conformational structure formed by the disulphide bonds between Cys6 and Cys48, and between Cys47 and Cys52 (epitope 1), Leu10-Val11-Asp12 (epitope 2), Val17-Cys18-Gly19-Asp20 (epitope 3), Arg21-Gly22-Phe23-Tyr24 (epitope 4) and Lys68-Ser69-Ala70 (epitope 5). Of these, the peptide containing epitope 5 showed the highest affinity to PcAb. The results indicated that our ELISA system combined recognition by epitope 2 of McAb and recognition by epitope 5 of PcAb to obtain its good specificity.
Journal of Endocrinology (1990) 125, 327–335
Luteal steroidogenesis and regression in the rat: Effects of human chorionic gonadotrophin and phospholipase A2 on cells and plasma membranes
Authors: Greenhalgh E. A. 
Published: December 2008

ABSTRACT
Progesterone production in vitro was measured in response to human chorionic gonadotrophin and phospholipase A2 using dispersed luteal cells from control and prostaglandin F2α (PGF2α)-treated rats. Highly purified luteal plasma membrane suspensions were prepared by partition distribution in dextranpolyethylene glycol, and membrane fluidity was measured by fluorescence polarization using the probe, trans-parinaric acid. Fluorescence polarization was highly dependent upon calcium, and was markedly affected by PGF2α treatment. No support was found for the theory that bulk membrane fluidity has a role in receptor or enzyme hindrance in the induction of luteal cell regression. However, membrane phase transitions induced by calcium interaction with anionic phospholipids and free radical damage may be involved in regression of the rat corpus luteum.
Journal of Endocrinology (1990) 125, 387–396
Luteal steroidogenesis and regression in the rat: Progesterone secretion and lipid peroxidation induced in luteal cells by human chorionic gonadotrophin, phospholipase A2 and prostaglandin F2α
Authors: Greenhalgh E. A. 
Published: December 2008

ABSTRACT
Mid-luteal phase (control) and mid-luteal phase luteal cell suspensions from rats given prostaglandin F2α (PGF2α) to induce luteal regression and killed 24 h later (P24-regressed) were incubated at 37 °C in serum-free medium. Progesterone secretion and lipid peroxidation induced by treatment with human chorionic gonadotrophin (hCG) alone or hCG plus phospholipase A2 and PGF2α were measured. Differences were demonstrated in progesterone secretion and lipid peroxide measurements between control and P24-regressed cell suspensions. The experiments suggested that malondialdehyde formation may be a useful indicator of luteal regression and cell death.
Journal of Endocrinology (1990) 125, 397–402
Feedback effects of growth hormone on anterior pituitary function in chickens
Authors: Lea R. W. , Harvey S. 
Published: December 2008

ABSTRACT
Circulating GH concentrations were suppressed 24 h after intracerebroventricular (i.c.v.) injection of native or recombinant DNA-derived chicken GH (rcGH) (10 μg in 4 μl vehicle) into the right lateral ventricles of conscious 6-week-old cockerels. Plasma concentrations of LH were suppressed within 1 h of i.c.v. administration of GH at doses of 1 or 10 μg, and remained suppressed for 24 h in birds injected with the highest concentration of GH. In contrast, concentrations of plasma prolactin were increased 24 h after i.c.v. administration of GH (10 μg). The i.v. administration of rcGH (at concentrations of 10 or 100 μg/kg) did not mimic the effects of i.c.v. injection of GH.
These results demonstrate central effects of GH on pituitary function in the domestic fowl.
Journal of Endocrinology (1990) 125, 409–415