bluuebunny/crossref_metadata_2025_split huggingface dataset:
Endogenous testosterone enhances growth hormone (GH)-releasing factor-induced GH secretion in vitro
Authors: Ohlsson L. , Isaksson O. , Jansson J.-O. 
Published: December 2008

ABSTRACT
The influence of endogenous gonadal steroids in male and female rats on basal and growth hormone-releasing factor (GRF)-stimulated GH secretion from perifused anterior pituitaries was studied. After 75 min of perifusion with basal medium, freshly dissected pituitaries were exposed to human GRF(1–44) (10 nmol/l) for 15 min. Neonatal (day 1–2) or prepubertal (day 25) gonadectomy of male rats suppressed baseline GH release (ng/min per mg dry weight) as well as GRF-stimulated GH release by 40–70%. This effect was slightly more pronounced in neonatally gonadectomized animals. In prepubertally gonadectomized male rats, the suppression of GH release was completely reversed by testosterone replacement therapy. In female rats, prepubertal gonadectomy did not affect GH secretion from perifused pituitaries. However, treatment of ovariectomized female rats with oestradiol reduced baseline and GRF-induced GH release to levels lower than those observed in sham-operated or vehicle-treated ovariectomized animals. The data suggest that testicular androgen secretion in adult male rats increases the pituitary GH release in response to GRF in vitro, whereas ovarian oestrogen secretion is of less importance for the GRF responsiveness of female rat pituitaries.
J. Endocr. (1987) 113,249–253
Secretion of LH in spontaneously hypertensive rats
Authors: Rodriguez-Padilla M. , Bellido C. , Pinilla L. , Aguilar E. 
Published: December 2008

ABSTRACT
Weights of testes, seminal vesicles, ventral prostate and pituitary, plasma testosterone and LH concentrations, pituitary LH content and concentration, the LH in-vivo response after LHRH administration (1 μg), and basal and LHRH-stimulated secretion in vitro were analysed in adult male spontaneously hypertensive (SH) and normotensive control (WKY) rats.
Spontaneously hypertensive rats showed: (1) testis and pituitary hypertrophy; (2) seminal vesicle and ventral prostate atrophy; (3) increased plasma testosterone and LH concentrations; (4) increased pituitary LH content and concentration; (5) unchanged net increase of plasma concentrations of LH 15 and 45 min after administration of 1 μg LHRH; and (6) increased basal LH secretion in vitro with a normal response to LHRH stimulation.
These results provide evidence that SH rats show increased LH secretion with a normal response to LHRH stimulation. The coexistence of high plasma concentrations of testosterone with seminal vesicle and ventral prostate atrophy suggest a reduction in the effectiveness of testosterone in these structures.
J. Endocr. (1987) 113, 255–260
Specific binding sites for gonadotrophin-releasing hormone, LH/chorionic gonadotrophin, low-density lipoprotein, prolactin and FSH in homogenates of human corpus luteum. II: Concentrations throughout the luteal phase of the menstrual cycle and early pregnancy
Authors: Bramley T. A. , Stirling D. , Swanston I. A. , Menzies G. S. , McNeilly A. S. , Baird D. T. 
Published: December 2008

ABSTRACT
Corpora lutea were obtained from 52 women undergoing laparotomy during the luteal phase of the menstrual cycle. In addition, stromal, thecal and granulosa cell preparations were obtained from seven women undergoing ovariectomy during the late follicular–preovulatory phase of the cycle. The specific binding of a 125I-labelled gonadotrophin-releasing hormone (GnRH) agonist [d-Ser(But)6] GnRH(1–9)-ethylamide (buserelin) and of human chorionic gonadotrophin (hCG), human FSH (hFSH), human prolactin (hPRL) and human low-density lipoprotein (hLDL) to tissue homogenates was measured under optimal conditions. Bound LH/hCG was estimated by elution with acid-citrate buffer, followed by radioimmunoassay of released hormone.
Binding of GnRH agonist, though variable, was highest in mid-luteal corpus luteum and high binding was also present in three out of four corpora lutea of pregnancy. Binding of LH/hCG increased significantly with luteinization, reaching maximal levels in the mid-luteal phase before falling significantly. Occupancy of LH receptors by bound LH was relatively constant throughout the luteal phase (10·7–35·3%), but occupancy increased to >90% in corpora lutea from early pregnancy. Binding of hFSH was variable, with only five out of 50 corpora lutea having binding greater than 10 pg/μg DNA. Similarly, hPRL binding varied markedly with only six out of 44 having binding greater than 50 pg/μg DNA. Binding of LDL was highest in the early- to mid-luteal phases of the cycle.
In corpora lutea from all stages of the menstrual cycle (excluding corpora albicantia), GnRH agonist binding was highly correlated with the levels of unoccupied and occupied LH receptors (P < 0·001; n = 49 and n = 48 respectively) and with LDL receptors (P< 0·002; n = 49). Binding of GnRH agonist was also correlated with PRL binding (P<0·05; n = 21) but not with FSH receptors (P>0·4; n = 25). In addition, LDL binding was associated with PRL (P< 0·005; n = 21) and FSH receptors (P<0·05; n = 25) and with endogenously bound LH (P<0·03; n = 48), but not with unoccupied LH receptors (P = 0·8; n = 49). Moreover, in corpora lutea from the mid-luteal phase, there was a strong association between GnRH agonist binding and LDL receptors (P<0·02; n = 23). The correlations between GnRH agonist binding and a number of important indices of luteal function suggest a physiological role for GnRH-like factors in the human corpus luteum.
J. Endocr. (1987) 113, 317–327
Receptors for lactogenic hormones in the ovine corpus luteum. II: Specific inactivation of ovine prolactin
Authors: Bramley T. A. , Menzies G. S. , McNeilly A. S. , Friesen H. G. 
Published: December 2008

ABSTRACT
Sheep corpus luteum homogenates and membrane fractions discriminate between 125I-labelled human GH (hGH) and ovine prolactin (oPRL). The present studies were designed to establish whether ovine luteal tissue possessed a prolactin-specific inactivating enzyme. Preincubation of sheep luteal microsomes and cytosol fractions with 125I-labelled hGH had little effect on the ability of the hormone to rebind to pig luteal lactogenic receptors. In contrast, sheep luteal tissue fractions markedly decreased the binding ability of 125I-labelled oPRL. However, despite the profound loss of receptor-binding activity, there was no change in protein-bound radioactivity, nor in the elution profile of 125I-labelled oPRL by gel chromatography on Sephadex G-100. Moreover, the disparity between 125I-labelled hGH and oPRL was not overcome by preincubation of sheep luteal membranes with protease inhibitors of differing specificities.
We conclude that the disparity between the binding of hGH and oPRL in ovine tissues was due to the selective inactivation of oPRL. However, the activity responsible did not degrade the hormone extensively, nor was its action blocked by a range of protease inhibitors.
J. Endocr. (1987) 113, 375–381
Vasopressin receptors influencing the secretion of ACTH by the rat adenohypophysis
Authors: Buckingham J. C. 
Published: December 2008

ABSTRACT
The effects of selective agonists and antagonists of type 1 (V1) and type 2 (V2) vasopressin receptors on the secretion of ACTH in vitro by segments of adenohypophysial tissue and in vivo in rats pretreated with pentobarbitone and chlorpromazine were studied in the presence and absence of the 41 amino acid-containing peptide, corticotrophin-releasing factor-41 (CRF-41). The non-selective vasopressin receptor agonist, arginine vasopressin (AVP) and the V1-receptor agonist, felypressin caused dose-related increases in ACTH release in vivo and in vitro but the V2-receptor agonist, desmopressin was only weakly active in this respect. Their actions in vitro were antagonized competitively by the V1-receptor antagonist, d(C2H5)2-AVP, but were unaffected by the V2-receptor antagonist, d(CH2)5-d-Iso2-Thr4-AVP. Arginine vasopressin, felypressin and desmopressins in concentrations considerably lower than those necessary to elicit directly the release of ACTH, potentiated, in a dose-related manner, the activity of CRF-41 in vitro. The potentiating effects were not antagonized by the V2-receptor antagonist or by low concentrations of the V1 -receptor antagonist. At a higher concentration, the V1-receptor antagonist reduced, but did not abolish, the potentiating effects of AVP and its analogues. However, at this concentration, it also exhibited weak intrinsic activity and, like the agonists, potentiated the response to CRF-41. The results suggest that the direct effect of AVP on ACTH release is mediated by V1-like receptors. The vasopressin receptors involved in the potentiation of CRF-41 activity appear to be different.
J. Endocr. (1987) 113, 389–396
INHIBITION OF FSH-STIMULATED GRANULOSA CELL FUNCTION BY A SYNTHETIC FRAGMENT OF THE PORCINE INHIBIN α-SUBUNIT: EVIDENCE FOR INVOLVEMENT OF GnRH RECEPTORS
Authors: Hillier S.G. , Tsonis C.G. , Wickings E.J. , Eidne K.A. 
Published: December 2008

ABSTRACT
The bioactivity of a synthetic peptide fragment which mimics the N-terminal sequence of the 134-amino-acid porcine Inhibin α-subunit (pl- α1-26-Gly27Tyr28-OH) was tested and compared with the bioactivity of GnRH in rat granulosa cell cultures. Granulosa cells from immature female rat ovaries were cultured with hFSH and testosterone to stimulate the production of cyclic AMP, progesterone and oestradiol. Addition of pl- α1-26-Gly27Tyr28-OH to the culture medium caused a dose-dependent suppression of all three parameters (ID50 700-1,000 nmol/l). GnRH caused similar but higher-potency inhibition (ID50 2-4 nmol/l). Suppression of granulosa cell function by both peptides was fully reversible by a synthetic GnRH antagonist. Moreover, specific binding of the porcine inhibin fragment to ovarian GnRH receptors was demonstrated by radioreceptor assay. This is evidence that the porcine inhibin α-subunit fragment suppresses FSH-induced rat granulosa cell function via a mechanism of action similar to that of GnRH.
Influence of a prolactin- and ACTH-secreting tumour on oestrous cyclicity, the pro-oestrous surges of LH and prolactin and ovarian hypertrophy in the rat
Authors: Krieg R. J. , Rogers J. P. , Seibel H. R. 
Published: December 2008

ABSTRACT
These studies were designed to investigate the effects of a prolactin- and ACTH-secreting tumour (7315a) on reproductive cyclicity, pro-oestrous surges of LH and prolactin and ovarian hypertrophy in the rat. Normal adult Buffalo rats, which are syngeneic to the 7315a tumour, were found to have a significant prooestrous prolactin surge and a relatively low-level preovulatory LH surge. Within 14 days of s.c. injection of dispersed tumour cells, a small tumour was detectable by palpation in one rat, but measurable tumours were not observed until day 18. The pro-oestrous surge of LH, but not of prolactin, was effectively suppressed by day 17. Cessation of reproductive cyclicity (anoestrus) was apparent within 19·4±1·1 days of injection of tumour cells. Removal of a single ovary showed that there was no change in ovarian weight before anoestrus in the tumour-bearing animals. Subsequent hypertrophy of the second ovary was augmented during the early stages of tumour development (days 8 and 13), and this corresponded to the unexpected finding that the gonadotrophin surges on days 8 and 13 were significantly increased when compared with controls. Ovarian hypertrophy was not significantly different from that in controls after suppression of the gonadotrophin surge (day 17). The results suggest that inhibition of the preovulatory LH surge might be a critical event in the tumour-induced cessation of reproductive cyclicity. The fact that pre-surge concentrations of prolactin did not increase substantially until the conspicuous onset of tumour prolactin secretion on day 21 indicated that the preovulatory LH surge might be inhibited by relatively low levels of tonically secreted prolactin.
J. Endocr. (1987) 114, 41–48
Modulation by endogenous opioid peptides of the secretion of LHRH from cockerel (Gallus domesticus) mediobasal hypothalamic tissue
Authors: Stansfield S. C. , Cunningham F. J. 
Published: December 2008

ABSTRACT
An in-vitro superfusion system was used to study the effects of the endogenous opioid peptides [Met]-enkephalin (and its long-lasting analogue [d-Ala2, Met]-enkephalinamide), [Leu]-enkephalin and β-endorphin and of the opiate antagonist naloxone, on the secretion of LHRH from the mediobasal hypothalamus of the cockerel. The effects of the compounds on both basal release of LHRH and on release stimulated by a depolarizing pulse of increased extra-cellular potassium ion (64 mmol/l) were investigated. None of the endogenous opioid peptides altered basal release of LHRH; however, both [Met]-enkephalin (10 μmol/l) and [d-Ala2,Met]-enkephalinamide (1 μmol/l) significantly (P<0·05) reduced the response to depolarization. Neither [Leu]-enkephalin nor β-endorphin (0·1–10 μmol/l) were effective. Naloxone (1 μmol/l) administered alone significantly (P<0·05) increased basal release of LHRH and abolished the inhibitory effects of [Met]-enkephalin and [d-Ala2,Met]-enkephalinamide on depolarization-induced release. These results suggest that the endogenous opioid peptides exert a tonic inhibitory influence on LHRH secretion by the mediobasal hypothalamus of the cockerel.
J. Endocr. (1987) 114, 103–110
The role of the hypothalamic β-adrenergic system in controlling the LH rise in short-term castrated rats
Authors: Al-Hamood M. H. , Gilmore D. P. , Wilson C. A. , Tuohy-Jones P. , Drummond S. , Gopalan C. 
Published: December 2008

ABSTRACT
Intraventricular infusions of adrenaline and various pharmacological agents acting on β-adrenergic receptor subtypes were carried out in rats orchidectomized 16 h previously. Infusions (10 μl) of solutions containing the drugs were administered under anaesthesia induced with alphaxalone and alphadolone. Levels of LH were measured in plasma collected immediately before and at predetermined intervals after the infusion.
The acute rise in LH levels after castration was increased still further by isoprenaline (a mixed β1- and β2-agonist), fenoterol (a β2-agonist) and atenolol (a β1-antagonist). In contrast, prenalterol (a β1-agonist) and (2RS,3RS)-3-isopropylamino-1-(7-methylindan-4-yloxy)butan-2-ol (ICI 118 551) (a selective β2-antagonist) were inhibitory to LH release. Adrenaline itself, salbutamol (another selective β2-agonist), propranolol (a mixed β-antagonist) and metoprolol (a β1-antagonist) did not significantly alter plasma LH concentrations at the doses administered. The stimulatory effect of isoprenaline on LH release was partially reduced when given together with ICI 118 551, but was not affected when administered simultaneously with atenolol. The inhibitory effect of ICI 118 551 was, however, prevented by concomitant administration with fenoterol, as was that of prenalterol when infused with atenolol. The results suggest that the hypothalamic mediation of the short-term changes in LH release in response to castration is exerted, at least in part, through the activation of a β2-stimulatory component and the suppression of a β1-inhibitory component.
J. Endocr. (1987) 114, 167–172
Effect of thyrotrophin on epidermal growth factor receptors in monolayer cultures of porcine thyroid cells
Authors: Atkinson S. , Kendall-Taylor P. 
Published: December 2008

ABSTRACT
Primary cultures of porcine thyroid cells, grown as monolayers, showed saturable binding of epidermal growth factor (EGF). Scatchard analysis resolved the binding to a high-affinity/low-capacity site (dissociation constant = 0·17 nmol/l, maximal binding capacity = 1·67 pmol/106 cells) and a low-affinity/high-capacity site. Preincubation of thyroid monolayers with TSH for 3 days caused an increase in binding of 125I-labelled EGF due to an increase in the number of receptors, with the binding affinity unchanged. This effect was dose-dependent within the range of TSH concentrations 0·01–100 mu/l. The same effect was seen with dibutyryl cyclic AMP (10–1000 μmol/l). When the protein synthesis inhibitor cycloheximide was included in the TSH preincubation, the increase in EGF binding was abolished. The TSH effect on EGF binding was not mediated by thyroid hormones, since neither thyroxine (T4) nor tri-iodothyronine (T3) at 01 nmol/l–10 μmol/l could mimic the effect of TSH, nor could antisera to T3 or T4 neutralize the effect of TSH. The concentration of extracellular iodide (10 nmol/l–10 mmol/l) had no effect on the binding of 125I-labelled EGF. The results demonstrate that TSH increases the number of receptor sites for binding of EGF to thyroid monolayers in vitro. This effect is dependent upon protein synthesis and is mediated by cyclic AMP but not by thyroid hormones or iodide. This effect on binding of EGF may contribute to the trophic action of TSH.
J. Endocr. (1987) 114, 179–184
Improvements in the determination of the turnover rate of plasma thyroxine in avian species: application to the Japanese quail
Authors: Cookson E. J. , Glover J. 
Published: December 2008

ABSTRACT
The disappearance of the thyroid hormone thyroxine (T4) from plasma in fully grown male Japanese quail can be described as a first order process with a rate constant of 0·178 ± 0·013/h (mean±s.e.m., n = 8), which represents a half-life of 3·90 h. A small amount of [125I]T4 in relation to total circulating T4 was injected i.v. into Japanese quail and plasma samples were taken at appropriate time-intervals for the determination of residual plasma radioactivity. The rate of disappearance of [125I]T4 was subsequently equated to the turnover rate of the endogenous hormone. Previous methods were modified to overcome problems arising from possible disturbance of plasma T4 metabolism, recirculation of radiolabelled iodide, and to purify the [125I]T4 from the plasma samples. By using labelled T4 of very high specific activity, the amount of [125I]T4 administered was kept much smaller than has been used in previous studies on Japanese quail, thus limiting any interference with plasma T4 dynamics. To minimize any disturbance of plasma T4 metabolism, only four blood samples were taken, at three-hourly intervals after the injection of [125I]T4. The rapid turnover of T4 produced a large amount of labelled inorganic iodide, the re-entry of which into the plasma T4 pool was inhibited by s.c. administration of sodium thiocyanate 1 h before injection of[125I]T4. Assay of the true [125I]T4 turnover was significantly improved over that used in previous studies by purifying the [125I]T4 from the plasma samples chromatographically. The samples were applied to small Sephadex G-25 columns with sodium hydroxide (0·1 mol/l) as the eluant. This simple procedure clearly separated the [125I]T4 from the other radioiodinated plasma components such as free iodide, non-hormonal iodinated proteins and triiodothyronine (T3), thus enabling a more accurate assessment of the residual labelled T4 concentration in the plasma and hence the T4 half-life.
The future application of this method to the study of plasma T4 turnover under various experimental conditions is discussed and the possible involvement of T4 turnover studies in the assessment of T4 to T3 conversion is considered.
J. Endocr. (1987) 114, 191–198
Forskolin and thyrotrophin stimulation of rat FRTL-5 thyroid cell growth: the role of cyclic AMP
Authors: Ealey P. A. , Ahene C. A. , Emmerson J. M. , Marshall N. J. 
Published: December 2008

ABSTRACT
The adenylate cyclase stimulator forskolin increases intracellular cyclic AMP (cAMP) in rat FRTL-5 cells within minutes and, after a lag phase of 20–24 h, an increase of cells in metaphase is seen. The dose– response relationships were similar in both systems, with significant increases in the number of metaphases observed at ∼0·1 μmol/l and a doubling of cAMP levels at 1 μmol/l, whilst doses of 0·1 mmol/l and above proved cytotoxic. An involvement of intracellular cAMP as a positive intermediate in cell division was further suggested by the finding that a low dose of forskolin (0·1 μmol/l) potentiated TSH stimulation of mitosis. Isobutyl methyl xanthine (IBMX), a phosphodiesterase inhibitor, also acted as a mitogen and potentiated TSH action. Moreover, the simultaneous inclusion of low doses of IBMX and forskolin additionally potentiated TSH stimulation of mitosis. An analogue of cAMP, dibutyryl cAMP, also stimulated mitosis and acted over a restricted dose range, with maximal stimulation at 1 mmol/l.
We conclude that cAMP may act as a positive signal for FRTL-5 thyroid cell proliferation.
J. Endocr. (1987) 114, 199–205
Effect of asymmetrical reductions of photoperiod on pineal melatonin, locomotor activity and gonadal condition of male Syrian hamsters
Authors: Hastings M. H. , Walker A. P. , Herbert J. 
Published: December 2008

ABSTRACT
This study investigated the relationship of two overt circadian rhythms, locomotor activity and melatonin synthesis in the pineal gland, by comparing their responses to asymmetrical reductions in photoperiod. Transfer of male Syrian hamsters from long to short daylengths led to an increase in the duration of both locomotor activity and the period of melatonin synthesis. Over the course of re-entrainment, the two rhythms were held in a stable phase relationship, and the direction of the switch did not influence the rate of decompression or the final phase relationships established after 8 weeks in short daylengths. Decompression of the activity rhythm was not influenced by pinealectomy. Exposure to short photoperiods caused gonadal regression and a consequent decline in serum testosterone levels from 10 to <1 nmol/l. The direction of the photoperiodic switch did not affect the time-course of gonadal regression. These data demonstrate the important influence of photoperiod upon the duration of the nocturnal peak of melatonin production by the pineal and also demonstrate that this effect is one example of a more widespread response of the circadian system. A qualitatively similar signal controls both locomotor activity and melatonin synthesis, although the neural basis of this common mechanism is unclear.
J. Endocr. (1987) 114, 221–229
Influence of streptozotocin-induced diabetes on the concentration of immunoreactive somatostatin in the retina and peripheral blood of the rat: effect of insulin treatment
Authors: Ariznavarreta C. , Fernandez-Durango R. 
Published: December 2008

ABSTRACT
Changes in somatostatin-like immunoreactivity (SLI) were examined in the retina and peripheral blood of diabetic rats treated with streptozotocin (STZ) and insulin. There was no change in retinal SLI content at 4 and 11 days after administration of STZ but, thereafter, SLI increased progressively in the diabetic animals by 220% at 18 days and 300% at 27 days. Plasma SLI levels increased by 500% at 11 days and maintained similar levels thereafter. Diabetic animals treated with insulin (3–5 i.u. daily) for 27 days showed a significant (P < 0·01) decrease of retinal and plasma SLI levels compared with untreated diabetic animals. It is concluded that there is a significant increase of retinal and plasma SLI levels in diabetic rats which tends to normalize after several days of insulin treatment.
J. Endocr. (1987) 114, 363–367