bluuebunny/crossref_metadata_2025_split huggingface dataset:
RNA synthesis in Leydig cells during sexual maturation in the rat: effect of LH
Authors: Valladares L. E. , Ronco A. M. , Pino A. M. 
Published: December 2008

ABSTRACT
The trophic action of LH on Leydig cells involves the triggering of a number of cellular events including changes in protein synthesis. This latter change has led a number of workers to postulate an effect of LH on RNA synthesis. A direct action of LH on RNA synthesis, however, has been difficult to assess.
The aim of the present work was to analyse the effect of LH on RNA synthesis in vitro during sexual development. Studies were performed using purified Leydig cells from rats of 20, 30, 40, 50, 60 and 90 days of age. The results obtained show that basal uridine incorporation into RNA increases in an age-dependent manner in rats from 20 to 60 days of age and then remains unchanged until 90 days of age. A stimulatory effect of LH on RNA synthesis was clearly demonstrated only in the youngest rats (20 and 30 days old). In order to differentiate the effect of LH on different RNA populations, the RNA synthesized by immature and mature rats was analysed using a poly(U)-Sepharose column. In 20-day-old rats, LH stimulated both unbound and poly(A) RNA, although a more marked effect was clearly demonstrated on the latter. On the other hand, LH had an identical effect on both unbound and poly(A) RNA obtained from Leydig cells of 60-day-old rats.
This stimulatory effect of LH on RNA synthesis in Leydig cells from immature rats seemed specific, since effectors which act on interstitial cells, such as LH-releasing hormone, [Arg8]-vasopressin and FSH (which may act on macrophages) did not modify RNA synthesis. It is concluded that LH stimulates RNA synthesis in rat Leydig cells and that this effect is expressed differentially according to sexual maturity.
J. Endocr. (1986) 110, 551–556
[3H]9-desglycinamide,8-arginine vasopressin: metabolism and in-vivo fate
Authors: Verhoef J. , van den Wildenberg H. M. , van Nispen J. W. 
Published: December 2008

ABSTRACT
Half-lives based on the disappearance of [3H]9-desglycinamide,8-arginine vasopressin ([3H]DGAVP) following in-vitro incubation in plasma were 1·7 h (dog), 5·8 h (rat) and > 12 h (man). For all three species, and particularly dogs, biotransformation of the peptide in plasma occurred predominantly through carboxypeptidase activities, leading to the accumulation of AVP-(1–7). Disappearance of [3H]DGAVP from rat blood after a single i.v. injection followed a biphasic decay with half-lives of 2·2 ± 0·8 (s.d.) min (distribution phase) and 14·4±1·2 min (elimination phase). The central and peripheral volumes of distribution were high and of the same order of magnitude, being 0·21 and 0·25 litres/kg respectively. Blood clearance values ranged from 36 to 45 ml/min per kg. In addition to [3H]AVP-(1–7), [3H]tyrosine was also found to be a major radioactive metabolite in blood. Compared with i.v. dosing, the s.c. route of administration for [3H]DGAVP resulted in longer-lasting peptide levels in blood which persisted for up to 4–5 h after injection. Maximal concentrations were reached at 7·5 min, whereafter they declined bi-exponentially with terminal half-lives of 31·1±8·7 min. The mean bioavailability for DGAVP was almost 100%, demonstrating virtually complete absorption from the s.c. injection site.
J. Endocr. (1986) 110, 557–562
Effects of various inhibitors of phenylethanolamine N-methyltransferase on pulsatile release of LH in ovariectomized rats
Authors: Coen C. W. , Gallo R. V. 
Published: December 2008

ABSTRACT
This study was undertaken to investigate whether hypothalamic adrenaline is involved in pulsatile LH release in rats. Various inhibitors of phenylethanolamine N-methyltransferase (PNMT), the enzyme which catalyses the conversion of noradrenaline to adrenaline, were administered to freely moving ovariectomized rats bearing an atrial cannula.
Blood samples were taken continuously from 09.00 to 11.00 h and from 14.30 to 17.00 h. The drugs were administered either at 11.00 h only or at both 11.00 and 14.00 h. The various treatments with the vehicle or an inhibitor of peripheral PNMT, SKF 29661, produced no decrease in any parameter of pulsatile LH release. A single injection of one of the central PNMT inhibitors, SKF 64139 or LY 134046, at 11.00 h had no effect on LH release, but when given at both times the drugs suppressed the mean LH level, pulse frequency and amplitude.
The effect of these drugs on the level of dopamine, noradrenaline and adrenaline in the hypothalamus (including preoptic area) was assessed. There was no effect on the concentration of the catecholamines after SKF 29661. None of the treatments with SKF 64139 or LY 134046 resulted in a change in the level of dopamine or noradrenaline; the double dose did, however, produce a significantly greater depletion of adrenaline than that which was achieved with the single injection.
These results suggest that the maintenance of normal LH pulses is dependent upon the presence of a sufficient level of hypothalamic adrenaline. The presence of at least 41% of the control level of hypothalamic adrenaline was compatible with the maintenance of LH pulses, but 30% or less of that level was insufficient for their normal occurrence. The effects of LY 134046 are particularly significant since this drug, unlike some of the other PNMT inhibitors, lacks α-adrenergic antagonist properties.
J. Endocr. (1986) 111, 51–59
Parathyroid hormone stimulation of the Na+/K+ pump in rat clonal osteosarcoma cells
Authors: De Luise M. , Harker M. 
Published: December 2008

ABSTRACT
A clonal line of osteoblastic cells from a rat osteogenic sarcoma (UMR 106–06), known to possess parathyroid hormone (PTH)-responsive adenylate cyclase, has been shown to increase its rate of K+ uptake mediated by a Na+/K+ pump after exposure to the hormone. The increase in pump activity was not associated with significant changes in K+ efflux or Na+ influx and would therefore be expected to alter intracellular levels of both Na+ and K+. The maximal (75%) increase in pump activity was noted at a PTH concentration of 100 μg/l and half-maximal stimulation at 1·9 μg/l. The effect appeared to be independent of the adenylate cyclase system, since a synthetic peptide antagonist of PTH activation of adenylate cyclase failed to prevent stimulation of the Na+/K+ pump. Similarly, prostaglandin E2, an alternative agonist of adenylate cyclase in these cells, had no effect on the Na+/K+ pump. This novel action of PTH on monovalent cation transport in osteoblast-like cells should provide a clearer insight into the mechanisms of hormone-induced bone resorption.
J. Endocr. (1986) 111, 61–66
Mechanism of restoration of ACTH release in rats with long-term lesions of the paraventricular nuclei
Authors: Dohanics J. , Kapócs G. , Janáky T. , Kiss J. Z. , Rappay G. , Lászlo F. A. , Makara G. B. 
Published: December 2008

ABSTRACT
The effects of lesions in the paraventricular nucleus (PVN) on the adrenocortical response to ether stress were investigated in neurohypophysectomized and intact rats. During the first 4 days after placement of lesions in the PVN, the corticosterone response to ether stress was almost completely inhibited. It then gradually increased and, within 4–6 weeks of surgery, was restored to about 60% of that in sham-operated rats.
Basal plasma concentrations of corticosterone were low in rats after placement of lesions in the PVN and/or after neurointermediate lobectomy (NILX). Corticosterone responses to ether stress were similar in groups submitted to PVN lesions and/or NILX, and lower than those in the appropriate sham-operated groups. In all lesioned groups, plasma ACTH concentrations after a combination of stressors (ether plus laparotomy) were also lower than those in the sham-operated groups.
Six weeks after lesioning of the PVN, immunoreactive rat corticotrophin-releasing factor-41 (rCRF-41) concentrations in stalk-median eminence (SME) extract fell to about 5% of that in sham-operated rats, while immunoreactive arginine vasopressin (AVP) concentrations did not change. Immunohistochemistry revealed a substantial decrease in rCRF-41 immunostaining of the median eminence 6 weeks after lesioning of the PVN, though randomly located clusters of stained terminals were still seen in the whole rostro-caudal extent of the median eminence. A mixture containing synthetic rCRF-41 and AVP, in proportions similar to those in SME extracts from sham-operated rats, caused significantly less release of ACTH from anterior pituitary cell cultures than did SME extracts from sham-operated rats. Extracts of SME from PVN-lesioned rats released as much ACTH as a mixture containing synthetic rCRF-41 and AVP in proportions similar to those in the SME extracts from PVN-lesioned rats. Extracts of SME from either PVN-lesioned or sham-operated rats did not cause a significant increase in the amount of ACTH released when preincubated with antisera to both rCRF-41 and AVP.
It is suggested that (1) the restoration of the adrenocortical reponse to ether stress, evident within a few days of placement of lesions in the PVN, occurs independently of neurohypophysial function; (2) the full corticosterone and ACTH response to ether or ether plus laparotomy stress requires not only an intact PVN but also an intact neurointermediate lobe; (3) SME extracts from sham-operated rats contain a factor(s) with the ability to potentiate the ACTHreleasing effect of rCRF-41 and AVP; and (4) the ACTH-releasing activity of SME extract obtained from rats with long-term PVN lesions is probably due to its remaininJ content of rCRF-41 and AVP.
J. Endocr. (1986) 111, 75–82
Effects of histamine H1- and H2-receptor antagonists on thyrotrophin secretion in the rat
Authors: Ulloa E. R. , Zaninovich A. A. 
Published: December 2008

ABSTRACT
The effects of histamine H1- and H2-receptor antagonists on the pituitary-thyroid axis were studied in normal and thyroxine (T4)-treated rats. Acute administration (120 min before the test) of the H2 antagonist cimetidine induced a significant (P<0·01) increase in the TSH response to TRH, whereas treatment with histamine (30 min before the test) or with the H1-receptor blocker diphenhydramine (120 min before the test) was without effect. Treatment with cimetidine or ranitidine (another H2-receptor antagonist) for 5 days induced a marked decrease in basal plasma TSH concentrations (P<0·01), with no changes in pituitary concentrations of TSH. Plasma prolactin concentrations were similarly decreased by cimetidine (P<0·01), though not by ranitidine. Neither antihistaminic altered pituitary prolactin concentrations. Despite decreasing basal concentrations of plasma TSH, cimetidine augmented the response to TRH above baseline values (P<0·01) in control rats as well as in animals with T4-induced suppression of plasma TSH. Administration of cimetidine or ranitidine for 5 days was followed by a reduced concentration of plasma T4 and tri-iodothyronine (T3) (P<0·05 and P<0·01 respectively), perhaps as a result of the declining plasma TSH levels. These results provide the first evidence for the reduction of plasma TSH concentrations by H2-receptor blockers, and may indicate that histamine can physiologically regulate TSH and prolactin secretion through H2 receptors in the anterior pituitary. The results, however, do not disprove a central action of histamine, since the decreased plasma TSH concentrations in the presence of low plasma T4 and T3 concentrations, and also the decrease in plasma prolactin concentrations induced by cimetidine, suggest reduced hypothalamic stimulation.
J. Endocr. (1986) 111, 175–180
Metabolic effects of a biphasic oral contraceptive preparation containing ethinyloestradiol and desogestrel on serum lipoproteins and apolipoproteins
Authors: Voorhoof L. , Rosseneu M. , Caster H. , De Keersgieter W. 
Published: December 2008

ABSTRACT
The effect of the administration of a biphasic oral contraceptive containing ethinyloestradiol and desogestrel on the distribution and composition of serum lipoproteins was studied in a group of 17 healthy female volunteers. The women were treated for a period of 6 months and compared with a control group of ten untreated volunteers.
The serum lipoproteins were fractionated by density gradient ultracentrifugation into very low density lipoproteins (VLDL), low density lipoproteins (LDL), and into the high density lipoprotein (HDL) subfractions 2 and 3 (HDL2, HDL3). Lipids and apolipoproteins were assayed in the various fractions. No modification of either the lipid or apolipoprotein concentrations was observed in the control group. In the treated group, sex hormone-binding globulin (SHBG) and cortisol-binding globulin (CBG), and the serum content of cholesterol, triglycerides, HDL-cholesterol, apolipoprotein A-I (apo A-I) and apolipoprotein A-II (apo A-II) increased significantly after 3 and 6 months. The cholesterol and apolipoprotein B (apo B) content of VLDL increased significantly after 3 and 6 months, but remained unchanged in LDL.
High density lipoprotein subfraction 2 (HDL2)-cholesterol was significantly increased after 3 and 6 months but apo A-I only after 6 months. Since apo A-II did not change, the apo A-I/A-II ratio increased significantly after 6 months of treatment. In the HDL3 fraction, the apo A-I increase was significant after 3 and 6 months, while the increase of apo A-II was significant after 6 months. The apo A-I/A-II ratio remained constant.
The major effects with this particular preparation were observed on the oestrogen-sensitive variables and especially on apo A–I synthesis. The progestational compound desogestrel does not seem to affect significantly the lipoprotein profile changes induced by the oestrogenic compound.
J. Endocr. (1986) 111, 191–196
A sex difference in endogenous opioid regulation of the posterior pituitary response to stress in the rat
Authors: Carter D. A. , Williams T. D. M. , Lightman S. L. 
Published: December 2008

ABSTRACT
The influence of endogenous opioids on the posterior pituitary response to stress was investigated by measuring plasma hormone levels in immobilized male and female rats following either acute naloxone treatment or prolonged morphine administration. Naloxone significantly potentiated the oxytocin and arginine vasopressin (AVP) response to immobilization, but in female rats only. The responses of morphine-treated male rats showed differences compared with vehicle-treated controls, although chronic morphine treatment did not reliably alter the oxytocin or AVP responses to immobilization in males or females.
In a further experiment to investigate the role of gonadal hormones in determining the sex difference in responsiveness to naloxone, it was found that acute naloxone treatment significantly potentiated the posterior pituitary response to stress in castrated male rats.
These results extend previous studies showing a sex difference in stress-induced secretion of posterior pituitary hormones, providing evidence of a sexual dimorphism in the endogenous opioid regulation of this response which is partly determined by circulating gonadal hormones.
J. Endocr. (1986) 111, 239–244
Effect of growth hormone-secreting tumours on skeletal muscle cellularity in the rat
Authors: McCusker R. H. , Campion D. R. 
Published: December 2008

ABSTRACT
Tumours secreting GH (GH1) or GH plus prolactin (GH3) were induced in young (1-week-old) and mature (17-week-old) female Wistar–Furth rats. Young animals were killed at 11 weeks and mature rats at 30 weeks of age. Induction of tumours increased serum GH concentrations and body and soleus muscle weights when compared with those of control rats. The soleus and extensor digitorum longus (EDL) muscles were examined in transverse section by electron microscopy. The percentages of myofibres with myonuclei and with satellite cell nuclei present in both the soleus and EDL muscles were generally greater in young rats with tumours than in young control rats. The percentage of myofibres in the EDL muscle with myonuclei present was higher in mature rats with GH1 tumours compared with age-matched controls. The presence of tumours did not affect the number of fibres in the soleus muscle of either young or mature rats. It was concluded that increased GH concentrations increased muscle weight by increasing the DNA content of myofibres and by myofibre hypertrophy. The rate of proliferation of satellite cells apparently exceeded the rate of incorporation of daughter nuclei into the fibres of the young tumourbearing rats when compared with that of young controls. Thus, the factors regulating satellite cell proliferation and nuclear incorporation into the myofibre do not appear to be directly coupled.
J. Endocr. (1986) 111, 279–285
The relationship between perfusion medium flow rate and steroid secretion in the isolated perfused rat adrenal gland in situ
Authors: Hinson J. P. , Vinson G. P. , Whitehouse B. J. 
Published: December 2008

ABSTRACT
Using the in-situ, isolated, perfused rat adrenal preparation, we have investigated the effects of changes in the rate of perfusate flow through the gland, brought about both mechanically and by the use of vasoactive agents, in the absence of known adrenocortical stimulants. Adenosine caused a significant increase in the rate of perfusate flow through the adrenal, with a concomitant rise in corticosterone, but not aldosterone, secretion. Adrenaline, on the other hand, caused a decrease in the rate of perfusate flow through the gland, accompanied by a decrease in the rate of steroid secretion. Futhermore, increases in the rate of delivery of perfusate to the gland, brought about by increasing the peristaltic pump rate, caused a large increase in corticosterone secretion, although aldosterone was unaffected. Neither adenosine nor a mechanically increased rate of perfusate delivery increased steroid secretion by collagenase-dispersed rat adrenocortical cells superfused on a Sephadex column. These results suggest the existence of hitherto unsuspected intraglandular mechanisms for the control of steroid secretion.
J. Endocr. (1986) 111, 391–396
Prostaglandin F2α-induced functional luteolysis: interactions of LH, prostaglandin F2α and forskolin in cyclic AMP and progesterone synthesis in isolated rat luteal cells
Authors: Kenny N. , Robinson J. 
Published: December 2008

ABSTRACT
The acute antigonadotrophic action of prostaglandin F2α (PGF2α) was examined in dispersed luteal cell preparations from immature superluteinized rat ovaries. Cell suspensions prepared by collagenase digestion and purification over a Percoll density gradient were incubated for 1 h in Eagle's minimum essential medium in the presence and/or absence of LH, PGF2α, N6,O2′-dibutyryladenosine 3′,5′-cyclic monophosphate (dbcAMP) and forskolin. Medium was assayed for total progesterone and adenosine 3′,5′-cyclic monophosphate (cAMP). Luteal cell preparations showed typical steroidogenic (progesterone) responses to LH, mimicked by both dbcAMP and forskolin. Whilst the threshold LH dose to increase cAMP synthesis was greater than that for progesterone (100 μg/l compared with 1 μg/l), 24 μmol forskolin/l was the threshold dose for both cAMP and progesterone responses. Furthermore, combined doses of LH and forskolin synergistically raised cAMP yet produced less than additive increases in progesterone. Similarly, combinations of dbcAMP plus forskolin produced less than additive progesterone increases. These data suggest that forskolin may not act as a simple mimic of LH.
Prostaglandin F2α dose-dependently inhibited forskolin-induced cAMP and progesterone synthesis and also inhibited progesterone synthesis induced by dbcAMP. These data suggest that the antigonadotrophic effect of PGF2α has more than one locus of action, i.e. it both inhibits an adenylate cyclase event associated with cAMP generation and blunts the cellular response to cAMP. The present uncertainty over the exact locus of forskolin's action within the adenylate cyclase complex limits further delineation of the inhibitory action of PGF2α on LH-responsive adenylate cyclase.
J. Endocr. (1986) 111, 415–423
Kinetic measurement of the urinary production rate of cortisol in male piglets: is the prerequisite 'collection until all label has disappeared' necessary?
Authors: Kraan G. P. B. , Chapman T. E. , Drayer N. M. , Colenbrander B. , Buwalda G. 
Published: December 2008

ABSTRACT
Urinary cortisol production rate (CPR) was calculated by two different methods in five male piglets (about 3 kg bodyweight) injected i.v. with 40–120 kBq tritiated cortisol ([3H]F). After administration of [3H]F, urine was obtained from four consecutive collections for the following 2 days, during which 80–100% of the label was recovered. Total radioactivity in the urine was measured and used to calculate the total rate constant of 0·115 ± 0·011 h−1 and, from this, the mean biological half-life (t½) of 6·0±0·6 h (s.d.; n = 4). It was found that the mass ratio of the two principal urinary cortisol metabolites tetrahydrocortisone (THE) and tetrahydrocortisol (THF) was strikingly less than 1·0 (0·4±0·1; n= 14), which is the reverse of that observed in older pigs, neonatal infants and man. To calculate CPR conventionally, the cumulative specific activities of THE and THF were calculated for the 2-day period of urine collection. The apparent mean CPR values on the basis of THE and THF were calculated as 11·5±1·6 (n = 5) and 12·8 ± 3·3 (n = 5) μmol/day respectively, and 12·1 ± 1·4 (n = 5) μmol/day for the average of THE and THF.
The second method for calculating CPR consisted of determining the masses of THE and THF (μmol) per fraction of dose (m/fd) (fd refers to the ratio of radioactivity in the metabolite and dose) at different times after administration of [3H]F. The calculated m/fd values, which are synonymous with the dose divided by the specific activities of the metabolites, and the different times of urine collection were analysed by linear regression. The resulting slope is equal to the CPR. The CPR derived by this method for the average of THE and THF, 10·1±0·91 μmol/ day was significantly (P<0·014) lower than that derived conventionally, 12·1 ± 1·40 μmol/day.
This second method may be used when CPR is determined in neonatal infants by means of non-radioactive, deuterated or 13C-enriched cortisol, where the extent of negative feedback by the relatively high dose of exogenous steroid on cortisol secretion must be kept as low as possible. This method also allows urine collections to be used at times when the tracer is still being excreted.
J. Endocr. (1986) 111, 439–448