bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rapid effects of parathyroid hormone(1–34) and prostaglandin E2 on bone blood flow and strontium clearance in the rat in vivo
Authors: Cochrane E. , McCarthy I. D. 
Published: December 2008

ABSTRACT
The vascular effects of noradrenaline, ATP, parathyroid hormone (PTH) and prostaglandin E2 (PGE2) were investigated in the rat. Additionally, the exchange of mineral ions between bone and blood was assessed by measuring strontium clearance, with the aim of investigating whether the vascular effects of these agents altered uptake of mineral ions or if this exchange could be changed independently of blood flow. Radioactive microspheres and 85Sr were used to establish bone blood flow and mineral clearance. Measurements of bone blood flow and arterial pressure were made in each animal and used to calculate vascular resistance. A measurement of 85Sr clearance was also obtained. Arterial blood pressure was significantly affected by noradrenaline (P ≤ 0·003) and ATP (P ≤ 0·015). Additionally, noradrenaline significantly (P ≤ 0·03) reduced bone blood flow. This decrease was related to a significant increase in vascular resistance. Arterial blood pressure and bone blood flow were significantly reduced by both bovine PTH(1–34) (P ≤ 0·001, P ≤ 0·02) and PGE2 (P ≤ 0·005, P ≤ 0·001). Vascular resistance to bone was increased by both agents but this was only statistically significant in the case of PGE2 (P ≤ 0·01). A significant (P ≤ 0·001) reduction in strontium was also produced by PGE2. In each group the relationship between bone blood flow and strontium clearance was then analysed. Only the PGE2-treated group had a slope of the regression which was statistically different from both the control animals and the other drug-treated groups. Treatment with PGE2 therefore resulted in a dose-related decrease in 85Sr clearance which was not related to the reduction in bone blood flow.
Journal of Endocrinology (1991) 131, 359–365
Calcium transport in the proximal convoluted tubule and loop of Henle of rats made diabetic with streptozotocin
Authors: Garland H. O. , Harris P. J. , Morgan T. O. 
Published: December 2008

ABSTRACT
In-vivo microperfusion was used to localize the reabsorptive defect responsible for the hypercalciuria of diabetes mellitus and to investigate possible causative factors. Unidirectional proximal calcium absorption was not significantly different in rats made diabetic with streptozotocin compared with controls, providing evidence against the involvement of this nephron segment in the phenomenon. Calcium absorption by the loop of Henle, was however, significantly (P<0·01) lower in diabetic animals (32·1 ±1·2 vs 40·4±0·6 pmol/min). Based on our knowledge of calcium movements within the loop, it is likely that the reabsorptive defect resides within the thick ascending limb. The calcium lesion was found to be independent of acute changes in intraluminal glucose concentration and could not be corrected by acute insulin treatment. The study also provides new information on the relationship between intratubular glucose and fluid movements in the rat nephron. In diabetic rats a proximal perfusate containing 30 mmol glucose/l resulted in fluid absorption comparable with that seen in control rats perfused with 5 mmol glucose/l. However, intraluminal glucose had a stimulatory effect on fluid absorption in the loop of Henle of diabetic rats (10·7 ±0·5 vs 7·9±0·4 nl/min; P<0·01).
Journal of Endocrinology (1991) 131, 373–380
Autoradiographical localization of oxytocin-binding sites in the guinea-pig ovary at different stages of the oestrous cycle
Authors: Zhang L. , Dreifuss J. J. , Dubois-Dauphin M. , Tribollet E. 
Published: December 2008

ABSTRACT
The discovery that oxytocin is synthesized and stored in corpora lutea of ruminants has fostered a renewed interest in the possible roles of oxytocin in ovarian function. In the present study we describe the distribution of binding sites for oxytocin in the guinea-pig ovary. Sections were reacted with a radioiodinated oxytocin antagonist (125I-labelled OTA) to yield autoradiograms on film. Specific binding sites for oxytocin were defined as those which bound 0·05 nmol 125I-labelled OTA/l and where 1 μmol non-radioactive oxytocin/1 displaced the radioactivity. 125I-Labelled OTA consistently labelled the ovarian stroma and the theca interna, but not the corpora lutea, the granulosa cells or the theca externa. The amount of 125I-labelled OTA bound to ovarian stroma and theca interna was high in animals killed during dioestrus, and low during and shortly after oestrus. These data suggest that the binding sites are regulated by steroid hormone levels and that in the guinea-pig ovary oxytocin could exert a role in follicular steroidogenesis, maturation or ovulation rather than in luteal function. Oxytocin-binding sites were also shown in the uterus but their numbers varied only slightly during the cycle.
Journal of Endocrinology (1991) 131, 421–426
Steroid control of uterine motility via γ-aminobutyric acidA receptors in the rabbit: a novel mechanism?
Authors: Majewska M. D. , Vaupel D. B. 
Published: December 2008

ABSTRACT
γ-Aminobutyric acid (GABA) is a regulator of uterine motility. Stimulation of GABAA receptors tonically inhibited contractions of rabbit uterine strips, while stimulation of GABAB receptors enhanced contractions. Steroids appeared to interact with GABAA receptors to modulate uterine contractility: tetrahydroprogesterone (THP) inhibited while pregnenolone sulphate (PS) increased contractions. THP rapidly antagonized the stimulatory effect of PS, but progesterone inhibited the contractions after a delay, suggesting that the known 'silencing' actions of progesterone on the uterus could be mediated via the metabolite THP, which potentiates the inhibitory function of GABAA receptors. This novel mechanisms may play a role in uterine function during pregnancy and parturition.
Journal of Endocrinology (1991) 131, 427–434
Steroidogenic enzyme activity in the rat testis following Leydig cell destruction by ethylene-1,2-dimethanesulphonate and during subsequent Leydig cell regeneration
Authors: O'Shaughnessy P. J. , Murphy L. 
Published: December 2008

ABSTRACT
Ethylene-1,2-dimethanesulphonate (EDS) rapidly destroys Leydig cells in the rat testis, although repopulation occurs within 5–7 weeks. In this study we have examined the activity of testicular steroidogenic enzymes after Leydig cell destruction and during regeneration. This was designed to measure the contribution of cells, other than Leydig cells, to steroidogenic activity in the testis, and to determine whether changes in steroidogenic enzyme activity during Leydig cell regeneration after EDS parallel those which occur during normal Leydig cell development. The enzymes studied are those responsible for androgen synthesis and metabolism in the testis.
Adult male Wistar rats (300–350 g) were injected with EDS (100 mg/kg, i.p.) and testicular steroidogenic enzyme activity was measured on days 0, 3, 7, 14, 21 and 35. On day 3, when no Leydig cells remain in the testis, cholesterol side-chain cleavage (CSCC) activity, per testis, declined to undetectable levels, while 3βhydroxysteroid dehydrogenase (3βHSD) and 17α-hydroxylase retained only 0·04 and 0·15% of control activity respectively. In contrast, 17-ketosteroid reductase (17-KSR) and 5α-reductase retained 33 and 10% of control activity respectively. On day 7 there was a further loss of 17-KSR activity (to 20% of control) but no change in other enzymes. The 17-KSR activity remaining on day 7 after EDS was contained almost exclusively in the seminiferous tubules, while the low 3β-HSD activity remaining was confined largely to the interstitial tissue. Other enzymes showed a more even distribution between the two compartments.
On day 14 after EDS there was a tenfold increase in 3β-HSD activity (compared with day 7), with no change in CSCC, 17α-hydroxylase or 5α-reductase and a further loss of 17-KSR (to 11% of control). Between days 14 and 21 there were marked increases in the activities of CSCC, 3β-HSD, and 17α-hydroxylase, while 17-KSR showed no change in activity from day 14. Activity of 5α-reductase increased between days 14 and 21 to levels greater than those seen in control animals. By day 35 the activities of all enzymes had returned to control levels.
The results show that, in the adult rat testis, the activities of CSCC, 3β-HSD and 17α-hydroxylase are confined, almost entirely, to the Leydig cells, and only 17-KSR shows significant activity in another cell type. During regeneration of Leydig cells after EDS the pattern of changes in enzyme activity is very similar to that seen in the normal development of the adult population of Leydig cells.
Journal of Endocrinology (1991) 131, 451–457
ADRENALINE STIMULATES CHOLESTEROL SIDE-CHAIN CLEAVAGE CYTOCHROME P450 mRNA ACCUMULATION IN BOVINE ADRENOCORTICAL CELLS
Authors: Ehrhart-Bornstein M. , Bornstein S.R. , Trzeclak W.H. , Usadel H. , Güse-Behling H. , Waterman M.R. , Scherbaum W.A. 
Published: December 2008

ABSTRACT
The effect of adrenaline on the accumulation of mRNA encoding cholesterol side-chain cleavage cytochrome P450 (P450scc) and cortisol secretion was studied in bovine adrenocortical cells in primary culture. Treatment of cultured cells with adrenaline resulted in a 2-fold increase in mRNA encoding P-450scc, as revealed by Northern blot analysis. Under these conditions the maximal stimulation with ACTH resulted in a 6-fold accumulation of mRNA encoding P450scc. The effect of adrenaline on the expression of P450scc was abolished by the ß-blocker propranolol, while propranolol had no effect on ACTH-induced P450scc mRNA accumulation. Adrenaline stimulated the secretion of cortisol in a dose-dependent manner with a median effective dose of 0.5 μmol/l. The adrenaline-stimulated cortisol secretion amounted to 42% of the effect of ACTH (0.1 nmol/l). Upon adrenaline treatment, cAMP concentration in the culture medium increased about 50-fold over the basal value. It is concluded that the stimulatory action of adrenaline upon cortisol formation requires ß-adrenergic receptors and is due, at least in part, to a cAMP-mediated increase in the accumulation of mRNA encoding P450scc.
Seasonal changes in plasma androgens, glucocorticoids and glucocorticoid-binding proteins in the marsupial sugar glider Petaurus breviceps
Authors: Bradley A. J. , Stoddart D. M. 
Published: December 2008

ABSTRACT
An investigation spanning two breeding seasons was carried out to examine endocrine changes associated with reproduction in a wild population of the marsupial sugar glider Petaurus breviceps, a small arboreal gliding possum.
Using techniques of equilibrium dialysis and polyacrylamide gel electrophoresis at steady-state conditions, a high-affinity, low-capacity glucocorticoid-binding protein was demonstrated in the plasma of Petaurus breviceps.
Equilibrium dialysis at 36 °C using cortisol gave a high-affinity binding constant of 95 ± 5·2 litres/μmol for a presumed corticosteroid-binding globulin (CBG) while the binding constant for the cortisol-albumin interaction was 3·5 ± 0·4 litres/mmol.
There was no difference between the sexes in the affinity of binding of cortisol to CBG; however, the cortisol-binding capacity underwent seasonal variation in both sexes. Progesterone was bound strongly to the presumed CBG while neither oestradiol nor aldosterone appeared to be bound with high affinity to P. breviceps plasma.
In the males, peaks in the plasma concentration of testosterone coincided with the July–September breeding season in both years. A significant inverse relationship was shown to exist between the plasma testosterone concentration and the CBG-binding capacity.
In both sexes an increase occurred in the plasma concentration of free cortisol during the first breeding season, a pattern which was not repeated in the subsequent breeding season, possibly due to a lower population density in that year.
Journal of Endocrinology (1992) 132, 21–31
Preferential release of tri-iodothyronine following stimulation by thyrotrophin or thyrotrophin-releasing hormone in sheep of different ages
Authors: Peeters R. , Buys N. , Vanmontfort D. , Van Isterdael J. , Decuypere E. , Kühn E. R. 
Published: December 2008

ABSTRACT
The influence of TRH and TSH injections on plasma concentrations of tri-iodothyronine (T3) and thyroxine (T4) was investigated in neonatal (injection within 0·5 h after delivery) and growing lambs and in normal, pregnant and lactating adult ewes (all 2 years old and originating from Suffolk, Milksheep and Texal cross-breeds). Neonatal lambs had higher levels of T3, T4 and GH compared with all other groups, whereas prolactin and TSH were higher in lactating ewes. In all animals, injections of TRH increased plasma concentrations of prolactin and TSH after 15 min but not of GH at any time. Small increases in T3 and T4 were observed in neonatal lambs, without any effect on the T3 and T4 ratio, after prolactin administration, whereas prolactin did not influence plasma concentrations of T3 or T4 in all other experimental groups. Similar results for thyroid hormones were obtained after TRH or TSH injections. It was therefore concluded that the effects observed after TRH challenge were mediated by the release of TSH. With the possible exception of neonatal lambs, plasma concentrations of T3 after administration of TRH or TSH were always increased before those of T4; the increase in T3 occurred within 0·5–1 h compared with 2–4 h for T4 in all experimental groups. This resulted in an increased ratio of plasma T3 to T4 up to 4 h after injection. It is concluded that, in sheep, TRH and TSH preferentially release T3 from the thyroid gland probably by a stimulatory effect of TSH on the intrathyroidal conversion of T3 to T4.
Journal of Endocrinology (1992) 132, 93–100
Serum half-life and in-vivo actions of recombinant bovine placental lactogen in the dairy cow
Authors: Byatt J. C. , Eppard P. J. , Veenhuizen J. J. , Sorbet R. H. , Buonomo F. C. , Curran D. F. , Collier R. J. 
Published: December 2008

ABSTRACT
The clearance rate of recombinant bovine placental lactogen (rbPL) from the blood serum of four lactating dairy cows was measured using a specific radioimmunoassay. Two animals were non-pregnant, while the other two were at approximately 120 days of gestation. The rbPL was administered as an i.v. bolus injection (4 mg total) via an indwelling jugular catheter. Blood samples were taken periodically for 180 min and assayed for rbPL. Analysis of the clearance curves for the bolus injection suggested a single-compartment model and a serum half-life of 7·25 min. In a second experiment with the same animals, following cessation of lactation, rbPL or bovine GH (bGH) were administered by s.c. injection (50 mg/day) for 5 consecutive days. Blood samples were taken twice per day during the treatment period and a 3-day pretreatment period. Samples were analysed for glucose, blood urea nitrogen (BUN), non-esterified fatty acids (NEFA), creatinine, insulin, insulin-like growth factor-I (IGF-I) and IGF-II, tri-iodothyronine (T3), progesterone and IGF-binding protein-2 (IGFBP-2) to determine whether rbPL mediates similar metabolic effects to those of bGH. Administration of bGH stimulated an increase in NEFA, glucose, T3 and insulin, whereas none of these variables was affected by rbPL. The plasma concentrations of IGF-I and IGF-II were both increased by treatment with rbPL but, to a lesser extent than occurred with bGH. Interestingly, BUN and IGFBP-2 concentrations were reduced equally by bGH and rbPL. These results suggest that rbPL does not necessarily act as a GH agonist but, rather, may have distinct effects on intermediary metabolism that could be mediated through another specific receptor.
Journal of Endocrinology (1992) 132, 185–193
Effects of C19 steroids on adrenal steroidogenic enzyme activities and their mRNA levels in guinea-pig fasciculata-glomerulosa cells in primary culture
Authors: Provencher P. H. , Tremblay Y. , Bélanger A. 
Published: December 2008

ABSTRACT
The present study examined the effects of steroids on steroidogenic enzyme activity in adrenal glands. Guinea-pig fasciculata-glomerulosa (FG) cells maintained in primary culture were exposed to steroids for 48 h. Although the treatment with androstenedione alone had no effect on 3β-hydroxysteroid dehydrogenase 4-ene-5-ene-isomerase (3β-HSD), 17-hydroxylase and 17,20-lyase activities, there was inhibition of 11-hydroxylase and 21-hydroxylase activities. When FG cells were exposed to 10 nmol ACTH/l for the last 24 h of incubation, ACTH alone had no effect on steroidogenic enzymes but, while combined with androstenedione, it further decreased 21-hydroxylase activity and stimulated 17-hydroxylase and 17,20-lyase activities. Cortisol, corticosterone, oestradiol and 11β-hydroxy androstenedione had no effect on steroidogenic enzyme activities while the inhibitory effect on 21-hydroxylase activity was only observed with androstenedione, testosterone and dihydrotestosterone. Addition of hydroxyflutamide, a pure antiandrogen, did not block the inhibitory effect of androstenedione on 21-hydroxylase and 11-hydroxylase activities. The reduction in oxygen tension from 19 to 2% which was aimed at examining the oxygen-mediated effects on steroidogenic enzymes, revealed that the reduction in 21-hydroxylase activity induced by androstenedione could not be prevented by low oxygen tension. An interaction of C19 steroids at the level of the enzymes is also suggested by our finding that androstenedione had no effect on basal and ACTH-stimulated steady-state 11-hydroxylase, 17-hydroxylase, 17,20-lyase and 21-hydroxylase mRNA levels. These results indicate that C19 steroids alter the adrenal steroidogenic enzyme activities in such a manner that C19 steroid synthesis is increased while glucocorticoid production is inhibited. The mechanism of action of C19 steroids does not involve gene expression for steroidogenic enzymes but probably a direct interaction with steroidogenic enzymes, namely 21-hydroxylase, 17-hydroxylase and 17,20-lyase. Our data suggest that C19 steroids may reduce the amount of 21-hydroxylase in the microsomal fraction which may have a major impact on the levels of microsomal P450 reductase available for 17-hydroxylase and 17,20-lyase activities.
Journal of Endocrinology (1992) 132, 269–276
Oxytocin stimulates LH production by the anterior pituitary gland of the rat
Authors: Robinson G. , Evans J. J. , Catt K. J. 
Published: December 2008

ABSTRACT
Gonadotrophin-releasing activity of oxytocin has previously been demonstrated in vitro and in vivo. This study investigated whether oxytocin is also able to induce LH accumulation in pituitary cells. Following trypsin digestion and mechanical dispersion, pituitary cells from female rats were incubated with oxytocin (100 nmol/l) for 24 h. LH release stimulated by oxytocin increased (P < 0·001) progressively during the incubation indicating a different secretory pattern from the more rapid but less sustained secretion stimulated by gonadotrophin-releasing hormone. Oxytocin also enhanced (P < 0·01) total LH accumulation in the incubation system (released plus cell contents) which was apparent after 7–11 h of stimulation. The release of LH stimulated by oxytocin was reduced by the protein synthesis inhibitor cycloheximide (10 μmol/l). However, cycloheximide did not completely block oxytocin-stimulated LH release; there remained some LH release above that seen in non-stimulated controls (P < 0·01) revealing the presence of a cycloheximide-resistant component in the release mechanism. Furthermore, accumulation of total LH in 24 h incubations was suppressed (P < 0·01) by cycloheximide.
The advancement in LH release which oxytocin has been shown to induce in vivo in pro-oestrous rats was accompanied by an early reduction of pituitary LH stores. However, the fall normally observed in LH content during the surge was markedly attenuated by the oxytocin treatment. Thus, loss of pituitary LH stores was less in oxytocin-treated rats than in saline-treated controls, even though net LH release into plasma was increased. Therefore, oxytocin stimulated the replenishment of LH stores.
Although the mechanism(s) remains to be defined and the relationships between in-vitro and in-vivo results are as yet uncharacterized, the present study demonstrates that oxytocin treatment stimulates LH production in both dispersed cells and intact pituitaries in situ.
Journal of Endocrinology (1992) 132, 277–283
Requirement of oestrogens for the sensitivity of prolactin cells to vasoactive intestinal peptide in rats and man
Authors: Pizzi M. , Rubessa S. , Simonazzi E. , Zanagnolo V. , Falsetti L. , Memo M. , Spano P. F. 
Published: December 2008

ABSTRACT
Vasoactive intestinal peptide (VIP) is a prolactin-releasing hormone which is involved in the multifactorial modulation of prolactin secretion in mammals. Intravenous injection of VIP (1 μg/kg) to fertile women increased plasma prolactin levels and heart rate and reduced diastolic pressure. The same treatment to menopausal women caused similar cardiovascular effects but did not modify plasma prolactin levels. In contrast, TRH (200 μg, i.v.) induced a significant increase in plasma prolactin levels in both fertile and menopausal women. The relevance of oestrogens in affecting VIP-stimulated prolactin secretion was evaluated in vitro by measuring prolactin release from pituitary cells of control and ovariectomized rats. The sensitivity of rat mammotrophs to VIP, but not to TRH, was completely suppressed 3 or 4 weeks after ovariectomy. Furthermore, implantation of rats with a silastic capsule containing oestradiol-17β during ovariectomy, preserved the cell responsiveness to VIP. The prolactin-releasing property of VIP was also restored when pituitary cells from ovariectomized rats were cultured for 3 days in the presence of 10 nmol oestradiol-17β/l before being used for prolactin release experiments. The present study shows that the ability of prolactin-secreting cells to respond to the stimulatory action of VIP requires high levels of circulating oestrogens, both in man and rats.
Journal of Endocrinology (1992) 132, 311–316
Effects of deglycosylation of human thyroperoxidase on its enzymatic activity and immunoreactivity
Authors: Giraud A. , Franc J.-L. , Long Y. , Ruf J. 
Published: December 2008

ABSTRACT
Thyroid peroxidase (TPO) is a glycoprotein enzyme which catalyses the iodination of thyroglobulin and the coupling of iodinated tyrosines. Human TPO (hTPO) is the microsomal antigen recognized by the autoantibodies in the serum of patients with autoimmune thyroid disease.
An active detergent-solubilized immunoaffinitypurified hTPO was deglycosylated, either by peptide N-glycosidase F (PNGase F) or by endo-β-N-acetylglucosaminidase H (endo H), and the enzymatic activity and immunoreactivity of the native and degylcosylated forms were compared. Electrophoretic controls and affinoblotting with concanavalin A showed that deglycosylation was not total and that it was more pronounced with endo H than with PNGase F. The enzymatic activity of hTPO was inhibited by endo H deglycosylation, but not by PNGase F deglycosylation; this inhibition was not due to aggregation and/or insolubilization of the molecule subsequent to deglycosylation. Immunoreactivity was monitored by enzyme-linked immunosorbant assay (ELISA) with 13 mouse monoclonal antibodies, rabbit polyclonal antibodies and antibodies from serum of patients with Hashimoto's thyroiditis. In contrast with enzymatic activity, immunoreactivity was not modified or was slightly enhanced (with four monoclonal antibodies) by deglycosylation.
The results indicate that strong, if not total, deglycosylation induces a modification of the tertiary structure of hTPO, which affects the enzymatic site but does not modify markedly the epitopes implicated in the recognition of the molecule by the antibodies tested.
Journal of Endocrinology (1992) 132, 317-323