bluuebunny/crossref_metadata_2025_split huggingface dataset:
The paracrine role of angiotensin in gonadotrophin-releasing hormone-stimulated prolactin release in rats
Authors: Kubota T. , Judd A. M. , MacLeod R. M. 
Published: December 2008

ABSTRACT
It is well known that lactotrophs are in close proximity to gonadotrophs in the lateral region of the pituitary gland, and thus there is interest in interactions between these two types of cell. The present study was undertaken to investigate the role of angiotensin II (AII) in gonadotrophin-releasing hormone (GnRH)-induced prolactin release, and to examine the effect of oestradiol on the paracrine interaction among anterior pituitary cells of young male rats. Over a 3-day period, one group of rats was injected twice with polyoestradiol phosphate (0·5 μg/g body weight; PEP-treated group), and a second with saline (control group). Their anterior pituitary glands were enzymatically dispersed and, subsequently, the cells were allowed to reaggregate for 48 h.
A 20-min perifusion with 100 nmol GnRH/1 increased (P<0·01) prolactin release from these anterior pituitary cell aggregates. The integrated value for prolactin release was 9·1 ±2·9 ng/107 cells. In the PEP-treated group, basal release of prolactin was greater than that in the control group (P<0·01). However, during exposure to GnRH, the integrated amount of prolactin release by the PEP-treated group (12·5 ± 4·8 ng/107 cells) was not significantly different from that of the control group, although in each individual experiment the GnRH-stimulated prolactin release from the PEP-treated cells was higher than that from the cells that had not been exposed to PEP. The release of angiotensin I (AI) from these perifused pituitary aggregates was significantly (P<0·01) increased by GnRH. In contrast, GnRH-stimulated release of prolactin was significantly (P<0·01) suppressed by 100 nmol saralasin/l, a specific AII antagonist, in both control and PEP-treated groups, whereas saralasin did not attenuate GnRH-induced LH release. GnRH-induced LH release was suppressed by PEP treatment during the first 2 min of perifusion, but enhanced throughout the remaining 18 min. In PEP-treated cell aggregates, the release of AI was increased during the later period. These data demonstrate that GnRH is capable of stimulating prolactin release through a mechanism that may involve the release of angiotensin.
Journal of Endocrinology (1990) 125, 225–232
Effect of long-term inhibition of gonadotrophin secretion by the gonadotrophin-releasing hormone agonist, buserelin, on sex steroid secretion and ovarian morphology in polycystic ovary syndrome
Authors: Macleod A. F. , Wheeler M. J. , Gordon P. , Lowy C. , Sönksen P. H. , Conaglen J. V. 
Published: December 2008

ABSTRACT
In order to investigate the effect of long-term suppression of the gonadotrophin axis in polycystic ovary syndrome, eight affected subjects were given s.c. infusions of gonadotrophin-releasing hormone (GnRH) agonist buserelin for 12 weeks. Hormone measurement and ultrasound studies were carried out weekly, from 6 weeks before to 12 weeks after administration of buserelin. An overnight dexamethasone-suppression test was carried out before and after treatment.
Maximal suppression of LH to below the lower limit of that in normal subjects occurred after 6 weeks of treatment with buserelin. Plasma testosterone and androstenedione fell to normal levels during the infusion but reached pretreatment levels during the follow-up period. There was no effect of buserelin on plasma dehydroepiandrosterone sulphate or sex hormone-binding globulin. Ovarian size decreased significantly during the infusion with the disappearance of cysts in six subjects. After cessation of buserelin therapy, there was rapid and spontaneous ovulation which occurred within 3 weeks in all subjects. The results suggest that treatment with this GnRH agonist facilitates ovulation in this condition.
Journal of Endocrinology (1990) 125, 317–325
Effect of angiotensins on electrogenic anion transport in monolayer cultures of rat epididymis
Authors: Wong P. Y. D. , Fu W. O. , Huang S. J. , Law W. K. 
Published: December 2008

ABSTRACT
Confluent monolayers cultured from the rat cauda epididymidis have been shown to respond to angiotensin I (AI) and angiotensin II (AII) when studied under short-circuit conditions and bathed on both sides with Krebs–Henseleit solution. Both the decapeptide AI and the octapeptide AII elicited transient increases in short-circuit current (SCC) when added to the basolateral as well as to the apical surfaces, with the effect of basolateral application greater than that of apical application. The maximal responses produced by AI and AII were similar with median effective concentrations of 20 to 80 nmol/l. The increase in SCC by AII was dependent upon extracellular Cl− and was inhibited by addition of a Cl− channel blocker, diphenylamine 2-carboxylate, to the apical surface. These patterns of activity suggest that the SCC responses to angiotensins result from electrogenic chloride secretion. Pretreating the monolayers with captopril (100 nmol/l), an angiotensin-converting enzyme (ACE) inhibitor, reduced the response to basolateral application of AI, but completely abolished the response to AI added apically. These results suggest that the response to apical addition of AI was due to conversion of AI to AII which interacts with apical angiotensin receptors. This conversion was mediated by ACE which has been detected in epididymal monolayers. Of the endogenous ACE activity, 86% was found to be inhibited by captopril (100 nmol/l).
Responses of the epididymal monolayers to angiotensins were mediated by specific angiotensin receptors. [Sar1,Ile8]-AII, a specific antagonist of the AII receptor, completely inhibited the responses to AI and All but had no effect on the responses to bradykinin and endothelin. The effects of All were mediated by eicosanoid formation since piroxicam, a cyclooxygenase inhibitor, inhibited the AII-induced increase in SCC. This is the first study to demonstrate an effect of angiotensin on epididymal functions. We propose that angiotensin formed locally in the epididymis may play a role in the regulation of electrolyte and fluid transport.
Journal of Endocrinology (1990) 125, 449–456
Purification of human pituitary LH and thyrotrophin by hydrophobic chromatography
Authors: Hiyama J. , Surus A. , Renwick A. G. C. 
Published: December 2008

ABSTRACT
A new preparative procedure is described for the efficient purification of LH and TSH from frozen human pituitary glands. LH and TSH were isolated simultaneously from crude preparations by hydrophobic-interaction chromatography followed by separation and purification by reverse-phase high-performance liquid chromatography in a single step. Highly purified hormones were prepared in good yields (45 mg LH and 20 mg TSH/1000 glands) and with high biological activities; the potencies of purified LH and TSH were 5·8 × NIH-LH-S1 equivalent in an ovarian ascorbic acid depletion assay and 7·1 U/mg against human TSH MRC Research Standard (T1 70/9) in the McKenzie assay respectively. Cross-contamination by other glycoprotein hormones was low.
Journal of Endocrinology (1990) 125, 493–500
OESTROGEN PRODUCTION BY THE GOAT MAMMARY GLAND: TRANSIENT AROMATASE ACTIVITY DURING LATE PREGNANCY
Authors: Peaker M. , Taylor E. 
Published: December 2008

ABSTRACT
Mammary tissue from goats had significantly higher aromatase activity at 148-149 days of pregnancy than earlier in pregnancy or during lactation. Aromatase activity was determined by production of 3H2O from [1 β–3H]androstenedione that was inhibited by 4–hydroxyandrostenedione. The time of maximum aromatization was during peak mammary output of oestradiol–17β described previously in vivo in the same species. Aromatase activity in the mouse mammary gland was low and no peak was observed in late pregnancy. It is concluded that the oestrogens produced by the mammary gland in the late–pregnant goat are formed by aromatization of androgens.
Immunohistochemical localization of androgen receptors with mono- and polyclonal antibodies to androgen receptor
Authors: Takeda H. , Chodak G. , Mutchnik S. , Nakamoto T. , Chang C. 
Published: December 2008

ABSTRACT
Rat, human, and mouse tissues were stained immunohistochemically using mono- and polyclonal androgen receptor antibodies. Monoclonal antibodies were raised in rats and used to stain human and mouse tissues; polyclonal antibodies were raised in rabbits and used to stain rat tissues. Frozen tissue sections were incubated with the appropriate androgen receptor antibody and staining was completed by the indirect avidin-biotin peroxidase method. A comprehensive survey of rat and mouse tissues was performed. Antibody staining was found exclusively in the nucleus of certain specific cell types, suggesting that the androgen receptor is a nuclear protein.
All male sexual organs in the rat showed strong positive nuclear staining for androgen receptor. Weaker positive reactions were seen in kidney, liver, adrenal cortex and pituitary gland. Furthermore, positive staining for androgen receptor was exhibited in skeletal, cardiac and smooth muscle cells, and central nervous tissue. Female reproductive organs also contained androgen receptor-positive cells. The spleen was found to be the only organ examined which did not stain for androgen receptor. The monoclonal antibody could also demonstrate androgen receptor-positive cells in a human prostatic cancer and in a prostate with benign hyperplasia. These data demonstrate the use of antibodies in revealing cellular/subcellular distribution of androgen receptor in target tissues.
Journal of Endocrinology (1990) 126, 17–25
Sex difference in growth hormone feedback in the rat
Authors: Carlsson L. M. S. , Clark R. G. , Robinson I. C. A. F. 
Published: December 2008

ABSTRACT
Growth hormone inhibits its own secretion in animals and man but the mechanism for this inhibition is unclear: both stimulation of somatostatin release and inhibition of GH-releasing factor (GRF) release have been implicated. We have now studied the GRF responsiveness of conscious male and female rats under conditions of GH feedback induced by constant infusion of exogenous human GH (hGH). Intravenous infusions of hGH (60 μg/h) were maintained for 3 to 6 h whilst serial injections of GRF(1–29)NH2 (0·2–1 μg) were given at 45-min intervals. The GH responses were studied by assaying blood samples withdrawn at frequent intervals using an automatic blood sampling system. We have confirmed that male and female rats differ in their ability to respond to a series of GRF injections; female rats produced consistent GH responses for up to 13 consecutive GRF injections, whereas male rats showed a 3-hourly pattern of intermittent responsiveness. In female rats, multiple injections of GRF continued to elicit uniform GH responses during hGH infusions, whereas hGH infusions in male rats disturbed their intermittent pattern of responsiveness to GRF, and their regular 3-hourly cycle of refractoriness was prolonged. We suggest that this sex difference in GH feedback may be due to GH altering the pattern of endogenous somatostatin release differentially in male and female rats. Such a mechanism of GH autofeedback could be involved in the physiological control of the sexually differentiated pattern of GH secretion in the rat.
Journal of Endocrinology (1990) 126, 27–35
Ontogeny of growth hormone (GH) binding in the domestic turkey: evidence of sexual dimorphism and developmental changes in relationship to plasma GH
Authors: Vasilatos-Younken R. , Gray K. S. , Bacon W. L. , Nestor K. E. , Long D. W. , Rosenberger J. L. 
Published: December 2008

ABSTRACT
The post-hatch ontogeny of hepatic GH binding and its relationship to GH plasma profile characteristics in male and female turkeys of slow- (RBC-2) and fast-growing (F; selected from RBC-2) genetic lines were determined. Specific binding of 125I-labelled recombinant chicken GH to crude hepatic membrane preparations (100 000 g pellet) was determined at 2, 4, 8, 14 and 24 weeks of age for both total (occupied plus free; 4 mol MgCl2/l pretreatment) and free (without MgCl2 pretreatment) binding sites. Characteristics of the plasma GH profile were measured at each age by serial blood sampling through indwelling jugular vein catheters.
When specific binding to either free or total sites was expressed on a whole organ basis (i.e. hepatic GH-binding capacity/bird), binding increased dramatically (P < 0·0001) with increasing age over both lines and sexes. Total binding capacity (free plus occupied sites) per bird was greater for females than for males at 24 weeks of age (P < 0·04), as birds reached sexual maturity, but did not differ between fast- and slow-growing lines at any age. Available binding capacity (free sites) per bird was greater for the faster growing F than RBC-2 line at the older ages when body size was most divergent (14 and 24 weeks of age; P < 0·01, P < 0·06 respectively), but did not differ between sexes.
Correlation analysis at individual ages revealed a progressive change in the nature of the relationship between hepatic GH binding, plasma GH and somatic growth. At 2 weeks of age, when growth velocity of these birds was high relative to later ages, there were no significant correlations among hepatic GH binding, plasma GH and somatic growth. Thereafter, the correlation between total binding capacity and plasma GH concentration progressed from positive (r = 0·34; P < 0·16) to no correlation (r = −0·01; P< 0·97) to increasingly negative, until at the oldest age studied (24 weeks), the correlation was strongly negative (r = −0·55) and significant (P < 0·03). At the older ages, hepatic binding became significantly correlated to measures of somatic growth.
These results indicate that no consistent relationship exists between hepatic GH binding and plasma GH status, over all ages, lines and sexes. Rather different relationships exist at different ages/physiological states. In the growth-divergent lines of turkeys studied here, measures of somatic growth are most strongly correlated with hepatic GH binding at later ages, after the early period of most rapid growth is past, and as mature body size and onset of sexual maturity are approached. The phenomenon of down-regulation of hepatic GH binding as birds approach sexual maturity was suggested by a significant negative correlation between total binding sites and plasma GH at that time.
Journal of Endocrinology (1990) 126, 131–139
Pubertal development and testicular function in the male growth hormone-deficient rat
Authors: Bartlett J. M. S. , Charlton H. M. , Robinson I. C. A. F. , Nieschlag E. 
Published: December 2008

ABSTRACT
The pubertal development of a novel GH-deficient mutant, the dwarf rat, has been evaluated. The establishment of normal spermatogenic function within small testes suggests that GH plays no role in spermatogenic function during puberty and adult life. However, a reduction in testicular size may reflect a reduced Sertoli cell population, suggesting that GH may be of importance in prepubertal testicular development.
Furthermore, marked differences between the homozygous dwarf rat and homozygous GH-deficient mouse mutants (e.g. Snell, Ames, pygmy and little mutants) have been demonstrated. It would appear that the GH deficiency in the rat mutant is far more specific for GH than those hitherto described in the mouse. In contrast to Snell dwarf mice mutants, pituitary and serum concentrations of FSH and LH are normal throughout pubertal development in the dwarf rat. Both spermatogenic function and seminal vesicle function develop normally, whilst in Snell dwarf mice spermatogenic function develops late in life and seminal vesicles remain infantile. Serum and testicular concentrations of androgen are also normal in dwarf rats. Homozygous dwarf rats have been shown to be fertile in previous studies; however, our observations suggest that despite spermatogenesis being qualitatively and quantitatively normal when assessed histologically, reduced testicular size seen in dwarf rats would lead to a reduced daily sperm output in these animals.
The dwarf rat represents a mutant in which the consequences of the selective depletion of GH may be studied on various endocrine systems. The reproductive axis appears to be only partially affected, at an early age, by GH deficiency.
Journal of Endocrinology (1990) 126, 193–201
Development of a new Leydig cell population after the destruction of existing Leydig cells by ethane dimethane sulphonate in rats: an autoradiographic study
Authors: Teerds K. J. , de Rooij D. G. , Rommerts F. F. G. , Wensing C. J. G. 
Published: December 2008

ABSTRACT
The formation of new Leydig cells in adult male rats was studied after the complete destruction of the original population by ethane dimethane sulphonate (EDS). Following administration of EDS, proliferating interstitial cells were labelled in a pulse-chase experiment by way of three [3H]thymidine injections on days 2, 3 and 4 after EDS administration. Some of the newly formed Leydig cells found 14 days after EDS administration were labelled with [3H]thymidine, indicating that these Leydig cells were derived from precursor cells, most likely mesenchymal cells, that had incorporated [3H]thymidine at days 2, 3, or 4 after EDS administration. At 21 days after EDS administration, the total number of Leydig cells (labelled plus unlabelled) had increased 7- to 16-fold compared with the number of cells that were present 14 days after EDS had been administered.
In a second series of experiments, [3H]thymidine was given 2 h before the rats were killed (short-term labelling experiment). In this experiment it was shown that the proliferative activity of the mesenchymal cells, which are presumed to be the precursors of the Leydig cells, after a considerable increase at day 2 after EDS administration, had returned to the control level at day 7. However, the total number of mesenchymal cells (labelled plus unlabelled) remained increased from 2 to 49 days after EDS administration. This indicated that the majority of the new Leydig cells which were formed from day 14 onwards probably did not derive from differentiating mesenchymal cells. The labelling index of the Leydig cells was approximately 100 times higher 21 days after EDS administration than that of the untreated controls, showing that many Leydig cells were formed by proliferation of the newly formed Leydig cells. Thereafter, the labelling index of the Leydig cells gradually decreased, whereas the total number of Leydig cells still increased threefold. At 49 days after EDS administration, the number of Leydig cells was approximately 80% of that in normal adult rats.
It is concluded that the regeneration of Leydig cells after EDS administration is the result of two successive waves of proliferation, namely of the precursor cells (mesenchymal cells) and of the newly formed Leydig cells.
Journal of Endocrinology (1990) 126, 229–236
Transcellular iodide transport and iodination on the apical plasma membrane by monolayer porcine thyroid cells cultured on collagen-coated filters
Authors: Nakamura Y. , Kotani T. , Ohtaki S. 
Published: December 2008

ABSTRACT
Isolated porcine thyroid follicular cells were cultured on a collagen-coated Millipore filter to form a monolayer. The monolayer could translocate 125I added in the medium beneath the filter (basal medium) into the medium above the monolayer (apical medium) and form an iodide concentration gradient of several-fold. Transcellular iodide pump activity was observed when the cells were cultured with TSH in the basal medium. In the absence of TSH, the translocation of iodide was very slow. The concentration of TSH required to activate the iodide pump was 0·1–0·3 mU/ml. Addition of ClO4− to the basal medium inhibited transcellular transport, whilst addition of ClO4− to the apical medium was much less effective.
Constituents labelled with 125I in the apical medium were analysed. The amount of protein-bound 125I measured by acid precipitation was 3–8% of the total radioactivity. The residual radioactivity was found to be iodide ion by paper chromatography. Further analysis by sodium dodecylsulphate–polyacrylamide gel electrophoresis revealed that most of the 125I-labelled protein was at the position of bovine serum albumin which had been added to the culture medium.
The monolayer culture of cells on collagen-coated filter would be a useful experimental system for analysing thyroid cell functions for which the cell polarity is essential.
Journal of Endocrinology (1990) 126, 275–281
Binding of the receptor for 1,25-dihydroxyvitamin D3 to the 5′-flanking region of the bovine parathyroid hormone gene
Authors: Farrow S. M. , Hawa N. S. , Karmali R. , Hewison M. , Walters J. C. , O'Riordan J. L. H. 
Published: December 2008

ABSTRACT
Receptors for 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3) were prepared from bovine parathyroid glands and incubated with fragments of DNA of the 5′-flanking region of the bovine parathyroid hormone (PTH) gene covering 1700 base pairs (bp) upstream of the initiation site. In filter binding assays, incubation of the DNA fragment spanning − 700 to + 50 bp with 200 μg cytosolic protein gave 288±63% (mean ± s.d.) of binding in the absence of protein. In contrast, there was no significant reaction with the −1350 to − 700 bp fragment, nor was there binding of the receptor to a fragment of DNA covering the coding region of the PTH gene. Substitution of bovine serum albumin for the receptor preparation did not induce binding to the − 700 to + 50 bp fragment. The receptor-binding site was further defined to −700 to − 100 bp as deletion of the − 100 to + 50 bp did not reduce receptor binding.
Reaction of receptors further purified by sucrose density ultracentrifugation with a monoclonal antibody in immunoblots revealed a single species with a molecular mass of approximately 50 000 Da, which was absent in preparations of cos-1 cells. Autoradiography following incubation of receptors immobilized on nitrocellulose filters with the −700 to + 50 bp fragment indicated a single reactive band coincident with the band in the immunoblot. The DNA fragment did not bind to filters containing preparations of cos-1 cells. Extraction of the receptors in the presence or absence of 1,25-(OH)2D3 (4 nmol/l) or the presence of KCl (150 mmol/l) in the incubation medium had no significant effect on DNA binding to the protein in this assay.
Autoradiography following incubation of immobilized receptors with the −700 to +50 bp, −485 to −50 bp, −700 to −100 bp and −700 to −485 bp fragments revealed a binding site for the receptor for 1,25-(OH)2D3 between −485 and −100 bp upstream of the initiation site in the bovine PTH gene.
Journal of Endocrinology (1990) 126, 355–359