bluuebunny/crossref_metadata_2025_split huggingface dataset:
Involvement of the adrenergic system on the release of prolactin and lactogenesis at the end of pregnancy in the rat
Authors: Jahn G. A. , Deis R. P. 
Published: December 2008

ABSTRACT
The part played by the adrenergic system on the release of prolactin and lactogenesis induced by prostaglandin F2α and the antiprogesterone RU 486 was studied in pregnant rats. Two doses of prostaglandin F2α (150 μg) administered at 08.00 and 12.00 h on day 19 of pregnancy induced, at 12.00 h on day 20 (24 h after administration), a significant increase in the serum concentration of prolactin, with a significant decrease in serum progesterone levels. These hormonal changes significantly augmented casein and lactose levels in the mammary gland. Treatment with RU 486 (2 mg/kg) at 08.00 h on day 19 augmented casein and lactose concentrations in the mammary gland at 12.00 h on day 20 without modifying serum concentrations of prolactin and progesterone. The adrenergic antagonists, propranolol (3 mg/kg), metoprolol (10 mg/kg), ICI 118 551 (200 μg/kg), idazoxan (100 μg/kg) and prazosin (10 mg/kg), were administered s.c. at 12.00 and 20.00 h on day 19 and 08.00 h on day 20 of pregnancy to intact rats or to rats previously treated with RU 486 or prostaglandin F2α. These adrenergic antagonists did not modify serum prolactin or progesterone levels in intact or RU 486-treated rats, but serum prolactin levels in the prostaglandin F2α-treated group were significantly reduced by treatment with propranolol, metoprolol or prazosin. In addition, propranolol and ICI 118 551 also decreased the casein and lactose concentrations in the mammary glands of RU 486- and prostaglandin F2α-treated rats, while the other compounds had no effect. We also studied the effect of adrenergic antagonists on the release of prolactin and lactogenesis induced by the physiological decrease in progesterone at the end of pregnancy. On day 21 of pregnancy at 18.00 h, serum progesterone levels in intact rats were lower than 40 nmol/l, while serum prolactin and casein and lactose concentrations in the mammary gland were higher compared with values measured at 12.00 h on day 20. Treatments with propranolol, metoprolol or prazosin administered at 20.00 h on day 20 and 08.00 and 14.00 h on day 21 of pregnancy were capable of significantly reducing serum prolactin concentrations while only propranolol decreased mammary casein and lactose. The effect of propranolol was not mediated through a reduction in serum placental lactogen measured by Nb2 lymphoma cell bioassay.
These results show that the adrenergic system participates, through α1 and β1 receptors, in the regulation of prolactin release induced by the decrease in progesterone in pregnant rats. They also show that β2-adrenergic receptors play a role in the induction of casein and lactose synthesis in the mammary gland.
Journal of Endocrinology (1991) 129, 343–350
Kinetic evidence for two components in the priming effect of LH-releasing hormone in the rat
Authors: Johnson M. S. , Mitchell R. 
Published: December 2008

ABSTRACT
The priming effect of LHRH on LH release from prooestrous rat hemipituitary glands in vitro was analysed by kinetic approaches. Concentration–response curves for LHRH-, K+- and ionomycin-induced LH release were constructed for initial exposure to the secretagogues and after 'priming' with a low dose of LHRH (100 pg/ml). These data were analysed by a non-linear curve-fitting programme to reveal the potency and maxima of the responses before and after priming. The parameters obtained from the curves fitted to the LHRH concentration–response curves showed that two changes had occurred as a result of priming. There was an increase in the maximum amount of hormone released and also a relatively greater ability for low concentrations of LHRH to cause release (increased potency). The data for K+ and ionomycin revealed only one change as a result of priming, an increase in the maximum amount of hormone available for release.
The data indicate that LHRH, after self-priming, releases more hormone by at least two routes, one represented by a general increase in stimulus–secretion coupling (which is available to K+ and ionomycin), the other a specific up-regulation of signal transduction by the LHRH receptor–effector system.
Journal of Endocrinology (1991) 129, 351–355
Meclofenamate inhibits prostaglandin E binding and adenylyl cyclase activation in human myometrium
Authors: Bernal A. López , Buckley S. , Rees C. M. P. , Marshall J. M. 
Published: December 2008

ABSTRACT
The effect of sodium meclofenamate on the binding of [3H]prostaglandin E2 ([3H]PGE2) to membranes from human myometrium was investigated. Meclofenamate inhibited the binding of [3H]PGE2 to high-affinity (dissociation constant 1·5 nmol/l) sites in a reversible dose-dependent manner (inhibition constant 11 μmol/l). The mechanism of inhibition was mainly competitive, but at high doses of meclofenamate (≥ 100 μmol/l) there was loss of PGE receptor sites. Of several PG synthesis inhibitors tested, only meclofenamate and, to a lesser extent, mefenamic acid had a significant inhibitory effect. PGE2 stimulated cyclic AMP generation in slices of human myometrium and this was inhibited by meclofenamate in a dose-dependent manner (50% inhibition occurred at 9 μmol/l). Again, this effect was specific for meclofenamate and fitted a competitive mechanism at doses in the range 1–10 μmol/l and a non-competitive mechanism at higher doses. The data show that meclofenamate, in addition to its traditional role as a PG synthesis inhibitor, affects directly PGE receptor binding and activation.
Journal of Endocrinology (1991) 129, 439–445
Metabolic clearance rate of testosterone in male epileptic patients on anti-convulsant therapy
Authors: Wheeler M. J. , Toone B. K. , Dannatt A. , Fenwick P. B. C. , Brown S. 
Published: December 2008

ABSTRACT
There are several reports which state that male epileptics on anti-convulsant therapy have reduced sexual activity. We and others have shown that, although total testosterone is raised, the free testosterone concentration is reduced in this patient population. This could be a result of an increased metabolic clearance rate (MCR) of testosterone, inadequate secretion of LH to stimulate testosterone synthesis or inappropriately low testosterone production by the Leydig cells. We have examined these possibilities by measuring the MCR of testosterone in 15 male epileptics on anti-convulsant therapy.
In this group of patients, the mean LH (9·3±5·9 IU/l) and sex-hormone binding globulin (SHBG) (54·5±22·9 nmol/l) concentrations were significantly greater than those of five normal control subjects (4·7±1·11 IU/l and 26·0 ±7·0 nmol/l respectively). Mean total testosterone concentrations of the two groups were not significantly different but the mean percentage of free testosterone and free testosterone concentration were significantly lower in the patient population (2·06±0·43 vs 2·98±0·27 and 0·56±1·1 vs 0·79±0·7 pmol/l). The MCR of testosterone was significantly lower in the patients (773±322 vs 1354±443 1/day) and showed a positive correlation with the percentage of free testosterone. Therefore, our results suggest that the lowered free testosterone in male epileptics on anti-convulsant therapy is not due to an increased MCR of testosterone. The increased LH concentration suggests primary hypogonadism. This, in turn, could be responsible for low free testosterone levels in the presence of normal testosterone.
Journal of Endocrinology (1991) 129, 465–468
Influence of protein nutrition on the response of growing lambs to exogenous bovine growth hormone
Authors: MacRae J. C. , Bruce L. A. , Hovell F. D. DeB. , Hart I. C. , Inkster J. , Walker A. , Atkinson T. 
Published: December 2008

ABSTRACT
Interactions between protein supply and the anabolic response to exogenous bovine (b) GH have been examined in two experiments using 28–35 kg lambs sustained entirely by intragastric infusion of volatile fatty acids (700 kJ/kg W0·75 per day) into the rumen and the casein (600 mg (low protein; LP) or 1200 mg (high protein; HP)/kg W0·75 per day) into the abomasum. Sheep received continuous i.v. infusions of bGH for 6 days in experiment 1 and for 18 days in experiment 2. Nitrogen balances were determined daily throughout both experiments and blood samples, from indwelling catheters, were assayed for GH, insulin-like growth factor-I (IGF-I), insulin and glucose.
Infusion of bGH increased plasma GH concentration by five- to sixfold in all animals. There was an increase in N retention in both HP and LP animals over the first 2–3 days of GH administration. HP animals sustained higher N retentions (31%; P < 0·05) throughout the GH administration but LP animals did not. In contrast, plasma IGF-I concentrations increased progressively over the first 72 to 96 h of GH administration in all sheep and thereafter remained significantly (P < 0·05) elevated until termination of the GH infusion. In lambs which received both HP and LP infusions in experiment 1 the increase in IGF-I concentration by day 6 of GH administration was significantly (P < 0·05) greater when they received the higher protein intake. Plasma insulin concentrations increased rapidly (P < 0·05) with the onset of GH administration to levels which were 2·5 (LP)- and 4·8 (HP)-fold greater than those observed in the pre-and post-GH periods. Glucose concentration also increased during GH administration (P < 0·05), by 35% in LP animals and by 58% in HP animals.
High protein availability appeared necessary to sustain a protein anabolic response where lambs received exogenous GH infusions, even though plasma IGF-I concentrations were elevated on both high and low protein treatments.
Journal of Endocrinology (1991) 130, 53–61
Studies on the testicular source of inhibin and its route of secretion in rams: failure of the Leydig cell to secrete inhibin in response to a human chorionic gonadotrophin/LH stimulus
Authors: Tilbrook A. J. , de Kretser D. M. , Clarke I. J. 
Published: December 2008

ABSTRACT
To determine whether Leydig cells produce inhibin in the ram, Leydig cells were stimulated by administering human chorionic gonadotrophin (hCG) or raising the levels of endogenous LH by an injection of gonadotrophin releasing hormone (GnRH). Plasma concentrations of testosterone increased in the 72 h after either a single injection (P < 0·05) or two injections (P < 0·01) of hCG. Plasma concentrations of inhibin were not significantly influenced by either one or two injections of hCG. Administration of GnRH (1 μg) caused an 11-fold increase in plasma concentrations of LH but did not influence concentrations of inhibin in either the jugular or testicular veins (pampiniform plexus). In contrast, concentrations of testosterone were increased by about fourfold in both jugular (P < 0·01) and testicular (P < 0·05) veins. The concentrations of inhibin in the testicular vein were 1·3-fold higher than in the peripheral plasma (P < 0·05) both before and following treatment with GnRH whereas the concentrations of testosterone were 18- to 21-fold greater than in peripheral concentrations.
In view of the difference in concentrations of inhibin between testicular and jugular veins, in a further experiment a sample was taken from the jugular vein, a vein located in the tunica vasculosa of the testis (testicular vein) and from a vein (spermatic vein) and lymph vessels located in the spermatic cord. The mean (± s.e.m.) concentrations of inhibin were highest in the testicular lymph (45·93±4·21 μg/l; P < 0·001) compared with the peripheral (4·14±0·31 μg/l), spermatic (8·0±1·17 μg/l) or testicular (6·4±0·82 μg/l) plasma. Plasma concentrations of inhibin were significantly higher in the spermatic vein than in the testicular vein (P < 0·05) and jugular vein (P < 0·01), and concentrations of inhibin in the testicular vein were significantly (P < 0·05) higher than in the jugular vein. There were no significant differences in the concentrations of testosterone in the spermatic vein, testicular vein or testicular lymph but the concentrations of testosterone in the peripheral plasma were significantly (P < 0·05) less than in the testicular plasma or lymph.
These results suggest that, in the ram, the Leydig cell does not respond to hCG or endogenous LH by secreting inhibin or by influencing other cells within the testis to secrete inhibin within the time-frame of these experiments. The low testicular to jugular differences in the concentration of inhibin and the high concentrations of inhibin in the testicular lymph suggest that the lymph may be an important route of secretion of inhibin from the testis in the ram.
Journal of Endocrinology (1991) 130, 107–114
Effect of oestradiol benzoate and tamoxifen on the growth of and induction of progesterone receptors in the uterus and mammary gland of immature pigs
Authors: Lin C. L. , Buttle H. L. 
Published: December 2008

ABSTRACT
Intramuscular injection of oestradiol benzoate (0·1, 1 or 10 μg/kg per day) and tamoxifen (0·1 or 1 mg/kg per day) to 6-week-old immature pigs for 7 days induced a dose-dependent increase in the wet weight of the uterus and in the total content of uterine DNA, RNA and protein. Both compounds also stimulated a dose-dependent increase in the concentration of progesterone receptors in uterine cytosolic extracts (in terms of either fmol/mg DNA or fmol/g uterus). The concurrent administration of tamoxifen with oestradiol benzoate provoked significant (P < 0·05) increases in total uterine protein and in the concentration of progesterone receptors (P < 0·01) compared with treatment with oestradiol benzoate alone. Hence tamoxifen is an oestrogen agonist in the uterus of immature pigs.
The effects of oestradiol benzoate and tamoxifen on mammary growth in immature pigs were assessed by image analysis of mammary sections across the gland (in a ventro-dorsal direction through the teat). Oestradiol benzoate at 10 μg/kg per day stimulated a fourfold increase in mammary duct area (P < 0·01), and tamoxifen, at doses of 0·1 or 1 mg/kg per day, stimulated a threefold increase (P < 0·05). Tamoxifen partially inhibited (P < 0·05) the effect of oestradiol benzoate. The concentration of progesterone receptors was found to be very heterogeneous in cytosol extracts of mammary tissue of immature pigs and independent of treatment with oestradiol benzoate and/or tamoxifen.
Journal of Endocrinology (1991) 130, 259–265
Serotoninergic stimulation of aldosterone secretion in the rat in vivo: role of the renin-angiotensin system
Authors: Davies E. , Rossiter S. , Edwards C. R. W. , Williams B. C. 
Published: December 2008

ABSTRACT
Serotoninergic control of aldosterone secretion in vivo was investigated in conscious rats with indwelling arterial cannulae. Serial blood samples were taken from the animals before and after i.p. administration of 1 ml (4 g/l) 5-hydroxytryptophan (5-HTP), the precursor of serotonin, or saline and they were analysed for 5-HTP, serotonin, 5-hydroxyindoleacetic acid, plasma renin activity (PRA), corticosterone, aldosterone, sodium and potassium concentrations. The role of the renin-angiotensin system was investigated in animals pretreated for 1 week with the angiotensin-converting enzyme inhibitor captopril (25 mg/day). 5-HTP caused a significant increase in all parameters within 45 min except for sodium and potassium. Saline administration showed no significant effect. Captopril pretreatment did not impair the increase in any parameter by 5-HTP, with the exception of the aldosterone response which was significantly attenuated, though not completely.
The results show that administration of 5-HTP, which increases serum serotonin levels, stimulates PRA, aldosterone and corticosterone secretion. Captopril pretreatment inhibits the aldosterone response, suggesting that the aldosterone stimulatory properties of 5-HTP require the presence of angiotensin II, although it is unclear whether it acts in a mediatory or permissive capacity. The failure of captopril to inhibit the aldosterone response completely suggests the involvement of other mechanisms such as the hypothalamo-pituitary adrenal axis or a direct action of serotonin on the adrenal.
Journal of Endocrinology (1991) 130, 347–355
The use of low doses of ACTH in the investigation of adrenal function in man
Authors: Crowley S. , Hindmarsh P. C. , Holownia P. , Honour J. W. , Brook C. G. D. 
Published: December 2008

ABSTRACT
We have investigated the adrenal response, in eight healthy adult men, to low doses of ACTH(1–24) in order to define a dose which will elicit a response similar to that obtained with the short Synacthen test. The studies were performed at 14.00 h and blood samples were withdrawn at 5-min intervals after an i.v. bolus injection of ACTH(1–24). The sampling interval was crucial in determining the timing of the peak response. Using sampling times of 0, 10, 15, 20, 25 and 30 min ensured detection of 47 out of 48 peaks. A dose-dependent rise in plasma cortisol concentration was observed with bolus injections of ACTH(1–24) between 30 and 250 ng/1·73 m2 body surface area. Increasing the dose to 500 ng/1 ·73 m2 (500 times less than that used in the short Synacthen test) elicited an increment of plasma cortisol concentration of 200 nmol/l or greater in all subjects. Pretreatment with dexamethasone (1 mg) did not alter the timing of the peak cortisol concentration but blunted the increase (pretreatment: median, 159 nmol/l; range 83–239; on dexamethasone; median 62 nmol/l; range 21–207; P = 0·04). These data suggest that a dose of ACTH(1–24) of 500 ng/1·73 m2 satisfies the criteria of the short Synacthen test and may provide a useful method of investigating adrenal function.
Journal of Endocrinology (1991) 130, 475–479
The purification and development of a radioimmunoassay for β-core fragment of human chorionic gonadotrophin in urine: application as a marker of gynaecological cancer in premenopausal and postmenopausal women
Authors: Lee C. L. , Iles R. K. , Shepherd J. H. , Hudson C. N. , Chard T. 
Published: December 2008

ABSTRACT
The β-core fragment of human chorionic gonadotrophin (hCG) is a major part of the immunoreactive hCG-like material found in the urine of normal pregnant women. Patients with non-trophoblastic gynaecological malignancies have been found to have raised levels of urinary β-core. We describe the purification of β-core, the preparation of a polyclonal sheep antiserum and the development of radioimmunoassay. The minimum detection limit of this assay was 0·025 μg β-core/l. There was no significant cross-reaction with the free α-subunit, hLH, hFSH and hTSH (<0·7%), and only partial cross-reaction with intact hCG and free β-subunit of hCG (6·9 and 18%). Within-assay variability ranged from 2·03 to 12·5% and between-assay variability from 2·25 to 13·4%. The assay was applied to urine samples from 92 normal non-pregnant premenopausal women, 54 normal postmenopausal women and 65 women with active gynaecological disease (47 postmenopausal and 18 premenopausal). In normal premenopausal women the values ranged from < 0·025 to 0·62 μg β-core/l (median 0·043 μg β-core/l). The values for normal postmenopausal women ranged from <0·025 to 0·64 μg β-core/l (median 0·26 μg β-core/l). Postmenopausal women with gynaecological malignancy had values which ranged from <0·025 to 4·0 μg/β-core/l (median 0·31 μg β-core/l); premenopausal women in this group had values which ranged from < 0·025 to 1·15 μg β-core/l (median 0·12 μg β-core/l). On molecular sieve chromatography, the material found in the urine of normal postmenopausal women showed the physicochemical characteristics of authentic β-core. However, the only detectable serum gonadotrophin was LH. Considering the homology and evolution of hCG from LH, postmenopausal β-core-like material could be derived from the degradation of β-LH resulting in a fragment with essentially identical physicochemical and immunological properties. The use of β-core assay as a tumour marker must take account of the fact that this molecule occurs in the urine of normal subjects, and that the levels are substantially raised in normal postmenopausal women.
Journal of Endocrinology (1991) 130, 481–489
Pulsatile LH secretion in streptozotocin-induced diabetes in the rat
Authors: Dong Q. , Lazarus R. M. , Wong L. S. , Vellios M. , Handelsman D. J. 
Published: December 2008

ABSTRACT
This study aimed to determine the effect of streptozotocin (STZ)-induced diabetes on pulsatile LH secretion in the mature male rat. LH pulse frequency was reduced by 56% and pulse amplitude by 54%, with a consequential decrease of 72% in mean LH levels 8 days after i.v. administration of STZ (55 mg/kg) to castrated Wistar rats compared with castrated non-diabetic controls. Twice daily insulin treatment completely reversed all parameters of pulsatile LH secretion to control values. Food-restricted non-diabetic controls, studied to distinguish the metabolic effect of diabetes from that of concurrent weight loss, demonstrated a 34% reduction in LH pulse frequency but no significant changes in LH pulse amplitude or mean LH levels compared with non-diabetic controls given free access to food. To distinguish whether the decreased LH pulse amplitude in diabetes was due to a reduction in either the quantity of hypothalamic gonadotrophin-releasing hormone (GnRH) released per secretory episode or to decreased pituitary responsiveness to GnRH, the responsiveness of the pituitary to exogenous GnRH (1–1000 ng/kg body weight) was tested in diabetic rats after castration, using a full Latin square experimental design. The net LH response (total area under response curve over 40 min following GnRH) was decreased by 33% (P=0·001) in diabetic compared with control rats. The decreased LH pulse frequency in STZ-induced diabetes therefore suggests that the metabolic effect of diabetes is to decelerate directly the firing rate of the hypothalamic GnRH pulse generator independent of testicular feed-back. These effects were fully reversed by insulin treatment and were only partly due to the associated weight loss. The impaired pituitary responsiveness to GnRH is at least partly involved in the reduction of LH pulse amplitude.
Journal of Endocrinology (1991) 131, 49–55