bluuebunny/crossref_metadata_2025_split huggingface dataset:
Testicular serotonin is related to mast cells but not to Leydig cells in the rat
Authors: Aguilar R , Antón F , Bellido C , Aguilar E , Gaytan F 
Published: December 2008

Abstract
Testicular serotonin (5HT) concentrations were determined by HPLC in the testes of rats treated neonatally with oestradiol benzoate (EB) and in adult rats treated with the Leydig cell cytotoxic ethylene dimethane sulphonate (EDS). 5HT concentrations were related to mast cell numbers. EB-treated rats showed an accumulation of mast cells in the testes at 35 and 70 days of age and increased 5HT concentrations in both the interstitial fluid and the testicular capsule, whereas no increases in 5HT concentrations or in the number of mast cells were found for the ventral prostate of these animals. On the contrary, 5HT concentrations were not related to the number of Leydig cells. In EB-treated rats, in which Leydig cells were nearly absent at 35 days of age, 5HT concentrations were significantly increased. Furthermore, EDS-treated rats did not show significant changes in 5HT concentrations, in spite of the elimination of Leydig cells. These data suggest that mast cells are a major source of serotonin in the rat testis.
Journal of Endocrinology (1995) 146, 15–21
Effects of sodium depletion on the response of rat adrenal zona glomerulosa cells to stimulation by neuropeptides: actions of vasoactive intestinal peptide, enkephalin, substance P, neuropeptide Y and corticotrophin-releasing hormone
Authors: Hinson J P , Kapas S 
Published: December 2008

Abstract
There are several neuropeptides, present in nerves supplying the rat adrenal zona glomerulosa, which have been shown to stimulate aldosterone secretion in the intact perfused rat adrenal preparation. The purpose of the present study was twofold: first, to determine whether these peptides acted directly on adrenocortical cells by examining their effects on collagenase-dispersed rat zona glomerulosa cells, and second, to investigate the likely physiological significance of these actions, by determining whether the responses of zona glomerulosa cells to neuropeptides were changed by prior sodium depletion.
Of the peptides tested, neuropeptide Y (NPY) and substance P had only a minor effect on aldosterone secretion, which was not substantially affected by sodium depletion. Corticotrophin-releasing hormone (CRH) had a significant stimulatory effect on aldosterone secretion, but neither the threshold concentration for significant stimulation nor the maximal response to stimulation were altered by prior sodium depletion.
Vasoactive intestinal peptide (VIP), on the other hand, had little effect on aldosterone secretion by cells from normal animals, but was a potent stimulus to aldosterone secretion in cells obtained from sodium-depleted animals. The response to the Met-enkephalin analogue, [d-Ala2-Met2]-enkephalinamide (DALA), was also significantly enhanced by prior sodium depletion. Experiments using the angiotensin II receptor blocker, saralasin, were carried out to determine whether the enhanced actions of DALA and VIP seen in sodium depletion may be a result of activation of angiotensin II receptors, known to be increased in sodium depletion. Saralasin did not affect the response to either peptide.
These data suggest that all the peptides tested may be able to stimulate aldosterone secretion. However, the data obtained with substance P, NPY and CRH do not support a major role for these peptides in the regulation of aldosterone secretion either under control conditions, or in sodium depletion. The finding that the responses to VIP and DALA were altered by sodium depletion suggests that the actions of VIP and opioid peptides may have physiological significance in the regulation of aldosterone secretion in response to sodium depletion. Furthermore, the observation that saralasin does not inhibit the responses to these peptides strongly suggests that they are not acting through angiotensin II receptors, and may indicate altered VIP- and opioid-receptor regulation in sodium depletion.
Journal of Endocrinology (1995) 146, 209–214
Hormonal control of insulin-like growth factor-I and growth hormone receptor mRNA expression by porcine hepatocytes in culture
Authors: Brameld J M , Weller P A , Saunders J C , Buttery P J , Gilmour R S 
Published: December 2008

Abstract
The effects of various hormones commonly added to hepatocyte culture media upon the expression of the GH receptor (GHR) and insulin-like growth factor-I (IGF-I) genes in cultured porcine hepatocytes were investigated. Preliminary investigations indicated that there was an absolute requirement only for insulin, with high losses of cell viability upon long term exclusion of insulin from the culture medium. The decline in GHR expression with time in culture was found to be less when high levels of glucose were included in the medium. Therefore the basal culture medium used in these studies was Williams' medium E supplemented with 0·2% (w/v) BSA, 5000 mg glucose/l and 100 nmol porcine insulin/l. The addition of dexamethasone (100 nmol/l) increased the expression of both GHR and IGF-I (class 1 transcripts only) mRNA (P<0·001 and P<0·05 respectively), and resulted in an increased responsiveness of IGF-I mRNA expression to GH (1 μg/ml), when the two were added in combination (although only class 1 transcripts were shown to be statistically significant, P<0·01). The addition of either thyroid hormone (1 nmol/l T3 or T4) alone also increased the expression of GHR mRNA (P<0·01) in addition to the dexamethasone stimulated expression, with T4 appearing to decrease IGF-I expression slightly (P<0·05) (either on its own or with T3). As with dexamethasone, the thyroid hormones increased the response of IGF-I mRNA expression to GH (1 μg/ml) when added in combination with GH (P<0·001). These observations demonstrate one possible mechanism for the interactions of glucocorticoids and thyroid hormones with the GH–IGF axis.
Journal of Endocrinology (1995) 146, 239–245
Long R3 insulin-like growth factor-I (IGF-I) infusion stimulates organ growth but reduces plasma IGF-I, IGF-II and IGF binding protein concentrations in the guinea pig
Authors: Conlon M A , Tomas F M , Owens P C , Wallace J C , Howarth G S , Ballard F J 
Published: December 2008

Abstract
We have tested whether an animal with substantial amounts of both IGF-I and IGF-II in circulation, such as the guinea pig, would respond to chronic IGF infusion in the same manner as the adult rat, which has negligible amounts of IGF-II in blood. Female guinea pigs of 350 g body weight were continuously infused for 7 days with recombinant guinea pig IGF-I or -II (120 or 360 μg/day) or long R3 IGF-I (LR3IGF-I) (120 μg/day), an analogue which has much reduced affinities for IGF binding proteins. IGF-I or IGF-II infusion led to substantial increases in plasma IGF-I or IGF-II respectively in comparison with vehicle-infused animals. Nevertheless, body weight gain, feed intake, feed conversion efficiency and carcass composition were not significantly affected by any treatment (significance was deemed to be P<0·05). Amongst the tissues examined only the fractional weight (g/kg body weight) of the adrenals was increased, and that only by the higher dose (360 μg/day) of IGF-I. However, the fractional weight of adrenals, gut, kidneys and spleen were significantly increased by LR3IGF-I, but again overall growth was not stimulated. A possible explanation for the lack of IGF-I effects is that total circulating IGF concentrations were not increased by these treatments. IGF-II significantly raised total IGF concentrations at the higher dose only. Plasma IGF-I was reduced by IGF-II infusion, as was plasma IGF-II by IGF-I infusion. LR3IGF-I treatment lowered both plasma IGF-I and IGF-II concentrations, a response probably related to a reduction in total plasma IGF binding protein (IGFBP), especially IGFBP-3, concentrations. We conclude that although the guinea pig is responsive to IGF treatment, the effects differ markedly from those elicited in rats.
Journal of Endocrinology (1995) 146, 247–253
Inverse control of growth hormone and prolactin secretion in clonidine-stimulated dairy cattle
Authors: Borromeo V , Berrini A , Möller F , Secchi C 
Published: December 2008

Abstract
Clonidine is a specific α-2-adrenoreceptor agonist that stimulates growth hormone (GH) release in animals and humans. This drug was used to study the GH and prolactin (PRL) secretory response in dairy cows and heifers. An i.v. infusion of 10 μg/kg body weight induced GH release to a peak concentration after 30–60 min, while 2 μg/kg had no effect on GH secretory patterns. Plasma PRL decreased significantly (P<0·01) starting 15–60 min after both doses of clonidine, this effect lasting up to 6 h. Clonidine significantly lowered plasma insulin (P<0·01) and raised plasma glucose (P<0·01). The changes in plasma GH, PRL, insulin and glucose differed significantly between doses, the 10 μg/kg dose being more effective (P<0·01). The results of our investigation in dairy cattle provide evidence of (i) an increase in GH release after 10 μg/kg clonidine; (ii) a concomitant decrease in PRL secretion, hence GH and PRL secretion in cattle appear inversely controlled; (iii) a significant difference between the effects of the 2 and 10 μg/kg doses and (iv) no relationship between the changes in plasma GH and PRL after clonidine and plasma hormone levels before treatment.
Journal of Endocrinology (1995) 146, 271–277
The effects of oestradiol and relaxin on extensibility and collagen organisation of the pregnant rat cervix
Authors: Cheah S H , Ng K H , Johgalingam V T , Ragavan M 
Published: December 2008

Abstract
The effects of exogenously introduced oestradiol-17β (E) and relaxin (RLX) on cervical extensibility and collagen organisation were tested in rats ovariectomised in late pregnancy. When the cervices were stretched in vitro by 1 mm increments, it was found that those from rats given E alone generated significantly higher tensions than those from control rats, while cervices from rats given both E and RLX had tensions similar to controls. Examination of cervical sections under the light microscope and ultra-thin sections under the electron microscope showed that the collagen fibres in the cervices from E-treated rats were highly organised, whereas those from animals given E+RLX and control animals were disorganised and dispersed. It was concluded that E decreased cervical extensibility, while RLX counteracted the effect of E to maintain a soft and easily extensible cervix.
Journal of Endocrinology (1995) 146, 331–337
Basal tail skin temperature elevation and augmented response to calcitonin gene-related peptide in ovariectomized rats
Authors: Kobayashi T , Ushijima O , Chen J-T , Shiraki M , Ohta T , Kiyoki M 
Published: December 2008

Abstract
Hyper-release of calcitonin gene-related peptide (CGRP) plays a direct and pivotal role in the induction of menopausal hot flushes (HFs), in which a drastic increase in skin temperature occurs. However, it is not possible to investigate whether CGRP induces skin temperature increase and whether skin temperature response to CGRP changes and contributes to the occurrence of HFs in postmenopausal women who are in oestrogen deficiency. By using rats' tail skin temperature (TST), a good marker to evaluate skin temperature regulation, we examined the effects of CGRP and calcitonin (3, 10 and 30 μg/kg, i.v.) on TST in female rats and further investigated the TST change induced by CGRP (10 μg/kg, i.v.) in ovariectomized (OVX) rats compared with that in sham-operated (Sham) rats. We found that CGRP, but not calcitonin, induced a TST increase in a dose-dependent manner and that the TST change induced by CGRP (0·6 ±0·2 °C for OVX rats vs 0·3 ±0·1 °C for Sham rats, P<0·05) and also the basal TST (26·0 ± 0·2 °C for OVX rats vs 25·5 ±0·1 °C for Sham rats) were significantly greater in OVX rats (P<0·05). Furthermore, treatment with oestradiol (30 μg/kg, s.c.) for 8 days partially inhibited the augmented TST response to CGRP in OVX rats and almost completely inhibited (P<0·05) the basal TST elevation, with the concomitant recovery of the serum oestradiol level to that in Sham rats. These results suggest that the augmented skin temperature response to CGRP and the elevation of basal skin temperature that are found in OVX rats, animals which are oestradiol deficient, may also occur in menopausal women and contribute to their HFs.
Journal of Endocrinology (1995) 146, 431–437
Thyroid glands: novel sites of growth hormone action
Authors: Hull K L , Janssens W C J , Baumbach W R , Harvey S 
Published: December 2008

Abstract
Thyroid hormones inhibit the synthesis and release of GH in avian species. This may represent a feedback mechanism, since GH enhances the peripheral production of tri-iodothyronine (T3). The possibility that GH may also have direct effects on thyroidal function was therefore investigated.
The basal and thyrotrophin-induced release of thyroxine (T4) from incubated chicken thyroid glands was not enhanced, however, in the presence of chicken GH. Contrarily, GH impaired T4 release in a dose-related way. These actions were probably mediated by specific receptors, since binding sites for radiolabelled GH were demonstrated on the plasma membranes of chicken thyroid glands. Expression of the GH receptor gene in these tissues was also demonstrated using a cRNA probe for the rabbit liver GH receptor, which specifically hybridized with RNA moieties of 4·4 kb, 2·7 kb and 1·0 kb. Moreover, reverse transcription of thyroidal RNA and its amplification in the presence of 3′- and 5′-oligonucleotide primers coding for the extracellular or intracellular domains of the GH receptor generated electrophoretically separable fragments of 500 bp and 800 bp respectively, as would be expected from analysis of the hepatic GH receptor cDNA sequence. Digestion of the 500 bp fragment with NcoI or EcoRI also produced moieties of expected size (350 bp and 150 bp or 325 bp and 175 bp respectively), as did BamHI or HaeIII digestion of the 800 bp fragment (yielding fragments of 550 bp and 275 bp or 469 bp and 337 bp respectively). Translation of the GH receptor mRNA was also indicated by the immunocytochemical demonstration of GH receptors in thyroid follicular and parafollicular cells, using a specific polyclonal antibody raised against the chicken GH-binding protein.
These results therefore provide evidence, for the first time, of GH receptor gene expression in thyroid tissue and the translation of functional GH receptors in thyroid glands. These results also demonstrate differential effects of GH on the extracellular concentrations of T3 and T4, which may permit subtle regulation within the somatotroph-thyroid axis.
Journal of Endocrinology (1995) 146, 449–458
Mechanisms of altered LH secretion in neonatally oestrogenized male rats
Authors: Pinilla L , Tena-Sempere M , Gonzalez D , Aguilar E 
Published: December 2008

Abstract
It is well known that the control of LH secretion depends on the steroid milieu during the postnatal period. In this study LH secretion was analysed in adult male rats injected neonatally with 500 μg oestradiol benzoate (1) after orchidectomy, (2) after selective elimination of androgens by destruction of Leydig cells with ethylene dimethane sulphonate (EDS), and (3) after removal in orchidectomized animals of Silastic capsules containing testosterone. In addition, (4) in vivo and in vitro LH secretion in response to LHRH agonist and antagonists, (5) the hypothalamic LHRH content, (6) the basal and stimulated in vitro LHRH release, and (7) the LH responses after administration of naloxone (2 mg/kg), α-methyl-p-tyrosine (α-MPT; 250 mg/kg), N-methyl-d-aspartic acid (NMDA, 15 mg/kg) or kainic acid (KA; 15 mg/kg) were also examined. Our data indicated that (1) the LH response after orchidectomy, after EDS administration and after removal of Silastic capsules containing testosterone was diminished in oestrogenized male rats, (2) the pituitaries from oestrogenized males retained responsiveness to LHRH, (3) hypothalamic LHRH content was reduced in oestrogenized males, but the hypothalamus from oestrogenized males released more LHRH than those of control groups both under basal conditions or after depolarization, (4) α-MPT decreased LH secretion only in oestrogenized males, and (5) NMDA and KA stimulated LH only in oestrogenized males. We conclude that in oestrogenized male rats the loss of sensitivity to the negative feedback action of testosterone on LH secretion was not due to decreased pituitary responsiveness to LHRH stimulation or to the inherent damage of LHRH neurones. In contrast, changes in the mechanisms governing LHRH release seem to be involved. A lack of activation of the excitatory noradrenergic and aminoacidergic systems seems to be part of the neurochemical basis of altered gonadotrophin secretion in neonatally oestrogenized male rats.
Journal of Endocrinology (1995) 147, 43–50
A 67 kDa protein mediates pituitary adenylate cyclase-activating polypeptide and vasoactive intestinal peptide-stimulated insulin secretion in a hamster clonal β-cell line
Authors: Kulkarni R N , Smith D M , Ghatei M A , Bloom S R 
Published: December 2008

Abstract
Insulin secretion is regulated by neural and neurohormonal factors. The report of nerves releasing pituitary adenylate cyclase-activating polypeptide (PACAP) – a 38 amino acid peptide – in the endocrine pancreas, suggests it may be important in modulating insulin release. We therefore carried out receptor-binding studies on membranes prepared from the glucose-responsive clonal β-cell line HIT-T15, and also examined the effects of PACAP38, PACAP27 – a C-terminal truncated form of the peptide – and vasoactive intestinal peptide (VIP) on insulin and islet amyloid polypeptide (IAPP) release. We showed by chemical cross-linking that PACAP and VIP stimulate secretion from the clonal cells by binding to a receptor with a molecular weight of 67 kDa (n=4). Binding was saturable when membranes were incubated with 125I-PACAP27 (Kd 1·2±0·2 nm; Bmax 415·7±35·3 fmol/mg; n=4) or 125I-VIP (Kd 1·3±0·3 nm; Bmax 354·8 ± 42·8 fmol/mg; n=4). We also demonstrated an increase in glucose-stimulated insulin (PACAP27, 366·6 ±25·8% PACAP38, 389·9 ±13·4%; VIP, 342·6± 16·1% of control; all at 1 μm, P<0·01 vs control) and IAPP release (PACAP27, 236·9 ±26·2%; PACAP38, 226·5 ± 10·9%; VIP, 242·9 ± 15·8% of control; all at 1 μm, P<0·01 vs control). Incubation of the cells with these peptides, for a duration of 12 h, in the presence of 5·5 mm glucose, did not alter the expression of insulin or IAPP. These findings suggest that PACAP and VIP stimulate secretion of insulin and IAPP by binding to a 67 kDa protein on clonal β-cells and do not alter the transcription of insulin and IAPP under the conditions tested.
Journal of Endocrinology (1995) 147, 121–130
Tumour necrosis factor a, interferon γ and dexamethasone regulate IGF-I-maintained collagen production in cultured human fibroblasts
Authors: Bird J L E , Tyler J A 
Published: December 2008

Abstract
We examined the effects of tumour necrosis factor α (TNFα) and interferon γ (IFNγ) on the production of collagen by human infant foreskin fibroblasts. Collagen synthesis was maintained in the presence of IGF-I so that cytokine effects could be examined in the absence of serum. TNFα inhibited IGF-I-maintained collagen production in a dose-dependent manner. Maximal suppression of 50% was attained at a concentration of 7·5 ng/ml. IFNγ also suppressed collagen accumulation in IGF-I-maintained cells, with a maximal inhibition to 55% at 375 U/ml. The rate of collagen formation relative to total protein production for secreted proteins was calculated. This value decreased from 10·3% for IGF-I-cultured cells to 6·2% and 8·4% with the inclusion of TNFα and IFNγ respectively, indicating that inhibition was selective for collagen. TNFα (5 ng/ml) and IFNγ (250 U/ml) together suppressed IGF-I-maintained collagen production to approximately 35%, with a decrease from 10·3% to 2·9% in collagen production relative to total protein. The inclusion of a serum-free period prior to the addition of TNFα to the cultures resulted in a further inhibition to 15% of control. This increase in inhibition was not seen if dexamethasone was present in the serum-free period prior to cytokine addition. These data showed that IGF-Imaintained collagen formation is suppressed by the proinflammatory cytokines TNFα and IFNγ, and that these interactions are influenced by dexamethasone. Proinflammatory cytokines interact in a complex manner with other serum factors to modulate IGF-I-stimulated extracellular matrix production and may have important roles in regulating tissue repair.
Journal of Endocrinology (1995) 147, 167–176
Urinary clearance of atrial natriuretic peptide in Pekin ducks
Authors: Gray D A 
Published: December 2008

Abstract
To quantify the renal excretion of atrial natriuretic peptide (ANP) in birds, synthetic ANP was infused intravenously into conscious Pekin ducks at rates of 10, 30 and 90 ng/kg per min for 30 min and the relationships between plasma and urine ANP concentrations were monitored by RIA. The infusions of ANP produced dose-dependent elevations in the plasma concentrations of the hormone; however, urinary concentrations and excretion rates did not change significantly from the basal values of 142·2 ±21·5 pg/ml and 26·4 ± 4·5 pg/min per kg respectively. The metabolic clearance rate of ANP remained constant at each infusion dose (approximately 200 ml/min per kg). The urinary clearance rates (<0·3 ml/min per kg) indicated that the fraction of ANP cleared from the blood via the urine was less than 0·2%. Clearly, excretion of intact ANP via this route is not a quantitatively important means of elimination for this hormone in birds.
Journal of Endocrinology (1995) 147, 211–215