bluuebunny/crossref_metadata_2025 huggingface dataset:
Dopamine affects angiotensin II-induced steroidogenesis by altering clearance of the peptide in man
Authors: Connell J. M. C. , Tonolo G. , Davies D. L. , Finlayson J. , Ball S. G. , Inglis G. , Fraser R.
Published: December 2008

Infusion of dopamine is reported to reduce the response of aldosterone to infused angiotensin II in sodium-deplete but not sodium-replete man. Six normal male subjects were infused with angiotensin II in graded doses (2, 4 and 8 ng/kg per min) with or without dopamine (1·0 μg/kg per min) during both dietary sodium repletion and depletion. The responses of both aldosterone and 18-hydroxycorticosterone to infusion of angiotensin II appeared to be reduced by dopamine in sodium-deplete, but not sodium-replete, subjects. However, when the relationships between plasma concentrations of angiotensin II and corticosteroid were examined it was evident that plasma concentrations of angiotensin II were lower when dopamine was infused concurrently with the peptide (P<0·05).

In a second study, six sodium-deplete males were infused with angiotensin II at a constant rate (6 ng/kg per min) while dopamine (or placebo) was given in graded doses (0·5,1 and 5 μg/kg per min). Renal plasma flow was estimated from total body clearance of para-aminohippuric acid. Overall, angiotensin II concentrations were lower during dopamine infusion compared with those during infusion of placebo (63·2 ± 9·7 (s.e.m.) vs 92·3±6·4 pmol/l; P<0·01) and this was associated with a 40% increase in effective renal plasma flow (627 ± 68 vs 451 ± 15 ml/min; P < 0·05); there again appeared to be a reduced aldosterone response during combined angiotensin II/dopamine infusion compared with that during infusion of angiotensin II alone (1003 ± 404 vs 1225± 146 pmol/l; 0·05<P<0·1).

Dopamine appeared to increase the metabolic clearance of infused angiotensin II, possibly by altering blood flow through vascular beds, such as renal, which degrade the peptide. This may partly explain the effects of dopamine on the response of the adrenal to infusion of angiotensin II in sodium-deplete man; the physiological role of dopamine in the regulation of corticosteroidogenesis remains speculative.

J. Endocr. (1987) 113, 139–146
Effect of tri-iodothyronine on protein turnover in rat hepatocyte primary cultures
Authors: Gallo G. , Voci A. , Schwarze P. E. , Fugassa E.
Published: December 2008

The effect of tri-iodothyronine (T3) on protein turnover was studied using primary cultures of rat hepatocytes. Protein synthesis was significantly stimulated in cells cultured for 6 days in the presence of T3 (1 μmol/l). Protein secretion into the culture medium was not affected by the hormone. Breakdown of long-lived proteins, the bulk of cellular proteins which are preferentially degraded through the autophagic lysosomal pathway, was significantly stimulated by the hormone. It is concluded that T3 elicits a general stimulation of protein turnover in cultured hepatocytes.

J. Endocr. (1987) 113, 173–177
Role of potassium in vasopressin-induced production of cyclic AMP in rat renal papillary collecting tubule cells in culture
Authors: Ishikawa S. , Saito T. , Kuzuya T.
Published: December 2008

The effect of potassium (K)-free medium on the stimulation of cyclic AMP (cAMP) production by arginine vasopressin (AVP) and forskolin was examined in rat renal papillary collecting tubule cells in culture. All experiments were performed in the presence of 3-isobutyl-l-methylxanthine (0·5 mmol/l). Cellular cAMP levels in response to 1 nmol and 0·1 μmol AVP/1 were 430·9 ± 42·1 (s.e.m.) and 501·8± 43·6 fmol/μg protein per 10 min respectively; these levels were significantly (P <0·01) higher than those in the vehicle-treated group (126·6 ± 23·3 fmol/μg protein per 10 min). The cellular cAMP response to 1 nmol AVP/1 was significantly attenuated after 24 and 72 h of exposure of cells to K-free medium, cellular concentrations of cAMP being 280·2 ± 37·1 and 233·0 ± 9·6 fmol/μg protein per 10 min respectively. The response of cAMP to AVP remained unchanged when the cells were preincubated with K-free medium for 1 h. Similarly, forskolin (20 nmol/l)-stimulated cellular cAMP production was also significantly impaired after 24 or 72 h of exposure of cells to K-free medium. When the cells preincubated in K-free medium were again exposed for 1 h to K-replete medium containing 5 mmol KC1/1, cellular cAMP production in response to AVP or forskolin recovered totally. Cellular protein and ATP content and cellular viability were not altered by exposure of cells to K-free medium for 24 h, and thus the impaired cAMP response to AVP or forskolin in the K-depleted cells was independent of altered cellular viability and source of ATP. The present results indicate that the K ion is an important factor for AVP– and forskolin-activated adenylate cyclase at the catalytic unit in the renal papillary collecting tubule cells.

J. Endocr. (1987) 113, 199–204
Role of cell–cell contact in the preservation of differentiation and response to thyrotrophin in cultured porcine thyroid cells
Authors: Yap A. S. , Bourke J. R. , Manley S. W.
Published: December 2008

Cultured porcine thyroid cells did not reassociate into functional follicles in the presence of TSH unless the initial seeding density was adequate. At 0·2 × 106 cells/35 mm diameter culture dish the cells rapidly formed a monolayer even in the presence of TSH (128 μu./ml), and radioiodide uptake was not significantly increased compared with that in control cells. Seeding densities of 1–3 × 106 cells/dish resulted in cultures which responded to TSH with follicular development and increased radioiodide uptake. A cell-free membrane fraction of thyroid homogenate restored the ability of cultures seeded at low densities to respond to TSH with development of follicular morphology and increased radioiodide uptake. Delaying the addition of TSH by 48 h markedly reduced the stimulation of follicular development and radioiodide uptake of cultures. Addition of membrane fractions, or an alkali-soluble fraction of membranes, at zero time improved the responses to TSH added after a 48-h delay. It was concluded that maintenance of differentiation and of TSH-responsiveness in cultured thyroid cells was influenced by cell–cell contact.

J. Endocr. (1987) 113, 223–229
Differences in the ovulation rate of the right or left ovary in unilaterally ovariectomized rats: effect of ipsi- and contralateral vagus nerves on the remaining ovary
Authors: Chávez R. , Cruz M. E. , Domínguez R.
Published: December 2008

The possible existence of peripheral asymmetry in the neuroendocrine mechanisms participating in the response of the ovary to gonadotrophins, and the participation of the vagus nerve, was investigated. At oestrus, the ovulation rate (number of ovulating/number of treated rats) of the left ovary in right unilaterally ovariectomized rats was lower than that in the right ovary in left unilaterally ovariectomized rats (42 vs 84%). No differences in the number of ova shed per ovulating animal nor in compensatory ovarian hypertrophy (COH) were observed. Bilateral section of the vagus nerve resulted in reduced COH only in those animals with the left ovary in situ (right unilaterally ovariectomized). Section of the left vagus nerve induced different effects depending upon which ovary was left in situ. When the left ovary was in situ an increase in ovulation rate, COH and number of ova shed was observed; however, when the right ovary was left in place the above three parameters decreased. Section of the right vagus nerve produced a decrease only in COH in both right and left unilaterally ovariectomized animals. It is concluded that in the unilaterally ovariectomized rat the right ovary seems more able to react to compensatory regulatory systems than does the left. The character of the information carried by the left and right vagus nerve is different.

J. Endocr. (1987) 113, 397–401
Changes in gonadotrophin-releasing hormone and LH in Japanese quail during the first few days of photostimulation
Authors: Creighton J. A. , Follett B. K.
Published: December 2008

Castrated Japanese quail responded to a single long day with a five- to eightfold increase in plasma LH levels. A rise in LH secretion appeared 19–24 h after dawn and LH levels were still increased 3 days later, despite the fact that the birds had been returned to a short daylength. Pituitary LH content decreased, reflecting these changes in secretion, although significant falls in content were only found 36–96 h after dawn, when LH secretion was maximal. Hypothalamic gonadotrophin-releasing hormone content was not altered. One interpretation of this is that increased synthesis of the peptide compensates fully for the increased secretion.

J. Endocr. (1987) 113, 419–422
Effects of thyrotrophin-releasing hormone on renal function in the rat
Authors: Garland H. O.
Published: December 2008

Standard renal clearance techniques were used to investigate the acute effects of TRH on kidney function in anaesthetized rats. A significant reduction in salt and water outputs, glomerular filtration rate and renal plasma flow was produced within 10 min of infusion of 12 μg TRH over 30 min. The rapidity of the response may suggest a direct effect of TRH on the renal vascular system.

J. Endocr. (1987) 113,445–448
Age- and sex-dependent stimulation of growth rate in rats by the adrenal inhibitor trilostane
Authors: Sillence M. N. , Rodway R. G.
Published: December 2008

The effects of the adrenal inhibitor trilostane were examined in male and female rats to determine whether growth rate could be improved by lowering circulating plasma corticosterone concentrations.

Dose–response studies revealed that in young female rats (125 g) trilostane lowered peak plasma corticosterone levels in a dose-dependent manner. In male rats plasma corticosterone concentrations were reduced only by very high doses of trilostane (200 mg/kg), while lower doses (2–8 mg/kg) actually increased them.

Five growth studies were conducted using a total of 90 rats. In female animals, daily injections of trilostane (10 mg/day) caused an age-dependent increase in growth rate ranging from 11% in 127 g rats to 30% in 164 g rats. In three out of four experiments using females, food intake was slightly increased by the drug. Food conversion efficiency was improved consistently by trilostane by up to 18%. Trilostane-treated females had significantly heavier adrenal glands and livers, but lighter kidneys than control rats. When a complete carcass analysis was performed on one experimental group, no significant differences were found. Carcass component weights relative to control values were: body weight (103%), body water (105%), fat-free solids (103%), carcass weight (103%), body length (103%), body fat (95%) and gut content (96%).

In male rats (160 g), daily injections of trilostane (10 mg) resulted in a steady and sustained depression of growth rate reflecting a similar fall in food intake, with no change in food conversion efficiency.

It is concluded that in older female rats growth rate is constrained by physiological concentrations of glucocorticoids. Younger females are either less sensitive to trilostane or to changes in plasma corticosterone levels. Male rats are less responsive to adrenal suppression by trilostane than are females of a similar age and do not exhibit an anabolic response to this drug.

J. Endocr. (1987) 113, 479–484
Inhibition of progesterone secretion by a 3β-hydroxysteroid dehydrogenase inhibitor in pregnant goats
Authors: Taylor M. J.
Published: December 2008

Epostane, an inhibitor of 3β-hydroxysteroid dehydrogenase, was administered to goats in late pregnancy in the presence or absence of concurrent treatment with prostaglandin synthetase inhibitors (indomethacin and diclofenac sodium) and the effect on steroidogenesis in the corpus luteum and adrenal cortex determined by measurement of peripheral concentrations of progesterone and cortisol respectively. Concentrations of both steroids were reduced to about 20% of pretreatment levels within 6 h of epostane administration. Cortisol concentrations subsequently increased about 24 h after epostane administration and returned to and exceeded pretreatment values, but progesterone concentrations remained suppressed until premature delivery, which occurred in all animals 44 ± 2 h (mean ± s.e.m.) after epostane administration. However, combined administration of epostane and prostaglandin synthetase inhibitor prevented the onset of labour in the majority of animals, but progesterone secretion in animals receiving this combined treatment did not differ from that in animals given epostane alone. It is concluded that progesterone withdrawal is an important component of the mechanisms which initiate parturition in the goat and that increased prostaglandin synthesis is essential for delivery in this species, but perhaps not for luteolysis.

J. Endocr. (1987) 113, 489–493
Storage and release of secretory granules in human prolactinomas: modification by bromocriptine
Authors: Landolt A. M. , Osterwalder V. , Landolt T. A.
Published: December 2008

Electron microscopic morphometric evaluation of the effects of bromocriptine on human prolactinomas during and after short-term parenteral (7 days) and long-term peroral (4–6 weeks) treatment showed that a reduction in size of prolactinoma cells occurs within a few days (half-time to maximum shrinkage, 2·2 days). The number of secretory granules discharged into the intercellular space increased after short-term treatment by a factor of three but the total volume of stored secretory granules did not change significantly. The total volume of cellular lysosomes, both primary and secondary, decreased significantly to about one-half of the pretreatment value. The amount of stored lipoids, end-products of lysosomal activity, decreased in specimens treated for 7 days, but returned to pretreatment levels in specimens treated for 4–6 weeks, suggesting that lysosomal material is discharged from the cells together with the secretory material.

J. Endocr. (1987) 113, 495–499
Plasma growth hormone, somatostatin, insulin and glucagon inter-relationships during infusion of human pancreatic growth hormone-releasing factor in young and adult ducks (Anas platyrhynchos)
Authors: Foltzer-Jourdainne Ch. , Harvey S. , Karmann H. , Mialhe P.
Published: December 2008

Human pancreatic GH-releasing factor (hpGRF) increased the concentrations of plasma GH when infused i.v. into immature ducks. A dose-dependent increase in plasma GH was observed within 10 min of the start of infusion and was maintained during the 30-min infusion period. Simultaneous infusion of somatostatin S-14 prevented the increase in plasma GH induced by hpGRF, but when the infusion had finished there was a rebound increase in plasma GH. Infusion of the highest dose of hpGRF (800 ng/kg per min) in adult ducks had no significant effect on plasma GH.

Plasma somatostatin concentrations were reduced during the infusion of hpGRF in young but not in adult ducks. This observation suggests that the stimulatory effect of hpGRF on GH secretion may be partly due to its inhibitory effect on somatostatin secretion. Infusion of hpGRF in ducklings also increased the concentrations of glucagon and decreased levels of insulin in the plasma. Peripheral plasma glucagon and insulin levels in adult ducks were unaffected by hpGRF infusion. These results indicate that in ducklings, hpGRF increases plasma GH and glucagon concentrations and lowers plasma somatostatin and insulin levels. In the adult, these hormonal responses to hpGRF are not maintained. The highly stimulatory effect of hpGRF on GH secretion in ducklings may explain why plasma GH concentrations are high in these birds.

J. Endocr. (1987) 114, 25–32
Involvement of opiate receptor subtypes in the modulation of LHRH secretion by the cockerel (Gallus domesticus) mediobasal hypothalamus in vitro
Authors: Stansfield S. C. , Cunningham F. J.
Published: December 2008

Using an in-vitro superfusion system, the relative importance of three distinct subtypes of the opiate receptor in the control of the secretion of LHRH from the mediobasal hypothalamus of the cockerel was investigated. Basal release of LHRH was increased by the antagonist naloxone, which shows some μ-receptor selectivity, in a manner which was reversed by the μ-receptor specific agonist [d-Ala2, N-Phe4-Gly-ol5]-enkephalin (DAGO) and the μ- and δ-specific agonist [d-Ala2,N-Phe4,Met(0)ol5]-enkephalin (FK 33–824). The †-specific agonist [d-Thr2,l-Leu5]-enkephalyl-Thr (DTLET) and the κ-specific agonist 1-methyl-2(3-thienylcarbonyl)-aminomethyl-5-(2-fluorophenyl)-H-2,3-dihydro-1,4-benzodiazepine (KC 6128; (+)-titfluadom) did not reverse the effect of naloxone. The δ-specific antagonist N,N-diallyl-Tyr-α-aminoisobutyricacid-Phe-Leu-OH (ICI 174,864) failed to influence basal release. Release of LHRH stimulated by increasing the potassium ion concentration of the superfusate to 48 mmol/l was reduced by DAGO in a manner which was reversed by naloxone, and by FK 33–824 in a manner which was reversed by both naloxone and ICI 174,864. The agonists DTLET and titfluadom did not affect stimulated release of LHRH. These results support the proposal that spontaneous release of LHRH is tonically inhibited by agonists acting through the μ-receptor whilst, in response to a stimulus, the δ-receptor, in addition to the δ-receptor, may be involved.

J. Endocr. (1987) 114,111–117
Lack of glucose-induced priming of insulin release in the perfused mouse pancreas
Authors: Berglund O.
Published: December 2008

Perfusion of the mouse or rat pancreas with 20 mmol d-glucose/l caused a biphasic release of insulin. The second phase was nearly constant in the mouse but rose in the rat. Repeated pulses of 8, 20 or 30 mmol d-glucose/l did not potentiate subsequent insulin responses in the mouse, whereas repeated pulses of 20 mmol/l did in the rat. When 20 mmol d-glucose/l was introduced through the mesenteric artery or aorta of the mouse, the pattern of insulin release was the same as when it was introduced through the coeliac artery. Thus, insulin secretion in mice differs from that in rats both in not showing an increasing second phase in response to continuous stimulation with glucose and also in not showing successive enhancement in the insulin response to repeated pulses of glucose.

J. Endocr. (1987) 114, 185–189
Modulation of plasminogen activation by glucocorticoid hormones in the rat granulosa cell
Authors: Harlow C. R. , Coombs R. J. , Hodges J. K. , Jenkins N.
Published: December 2008

Granulosa cells from immature rats primed with diethylstilbestrol (DES) showed a fivefold rise in the activity of secreted plasminogen activator (PA) in response to human FSH. The dose giving 50% of the maximum response (ED50) was 10 ng/ml. Glucocorticoid hormones significantly suppressed PA activity in both control cells and cells stimulated with FSH (ED50 = 50 nmol dexamethasone/l; 1 μmol corticosterone/l). Cortexolone (2·5 μmol/l) significantly ameliorated this suppression, indicating that the response to glucocorticoids is receptor-mediated. These data, together with the time delay required for glucocorticoids to take effect (5 h), suggest that glucocorticoids induce the production of a specific PA inhibitor in granulosa cells.

J. Endocr. (1987) 114, 207–212
Ovine allantoic fluid inhibition of prostaglandin synthesis in cotyledonary microsomes
Authors: Rice G. E. , Wong M. H. , Ralph M. M. , Thorburn G. D.
Published: December 2008

Inhibition of microsomal prostaglandin (PG) biosynthesis by allantoic fluid, obtained from ewes at 80–120 days of gestation, was examined. Inhibition of cotyledonary microsomal PGE2 and PGF2α biosynthesis by lyophilized allantoic fluid occurred in a dosedependent manner. The concentration of allantoic fluid required to inhibit PGE2 and PGF2α production by 50% averaged 17·9 ± 3·2 (s.e.m.) mg dry weight/ml (n = 5). Microsomal PG biosynthesis was markedly enhanced by the addition of arachidonic acid (30 μmol/l). Synthesis of PGE2 and PGF2α was increased to 245 ± 65% and 184±14% of control (P<0·05, n = 5) respectively. Treatment of cotyledonary microsomes with porcine phospholipase A2 (PLA2; 0·125 units/ml) also stimulated PG synthesis, PGE2 increasing to 216 ± 27% and PGF2α to 172 ± 14% of control (P<0·05, n=5) respectively. Allantoic fluid (20 mg dry weight/ml) inhibited arachidonic acid-stimulated PG synthesis (PGE2 by 48·6 ± 13·8% and PGF2α by 44·2 ± 7·7%) and PLA2-stimulated PG synthesis (PGE2 by 60·6±11·6% and PGF2α by 74·8 ± 8·5%). Allantoic fluid, however, did not affect PLA2-stimulated release of arachidonic acid from microsomes, thus negating the possibility that allantoic fluid suppresses PG synthesis by inhibiting PLA2 activity. These data indicate that allantoic fluid inhibits PG production at the level of PG synthase enzymes. Prostaglandin inhibitor(s) in allantoic fluid may play a role in maintaining uterine quiescence throughout gestation and its withdrawal, at term, may be involved in the initiation of labour.

J. Endocr. (1987) 114, 295–300
Growth hormone secretory profiles in conscious female rats
Authors: Clark R. G. , Carlsson L. M. S. , Robinson I. C. A. F.
Published: December 2008

An automatic method for repetitive microsampling of blood from conscious animals was used to obtain detailed GH secretory profiles from normal female rats, which were compared with those in males and ovariectomized females. Female rats showed a highly variable GH secretory pattern, with sustained periods of low, almost continuous secretion, followed by very rapid bursts of high amplitude and short duration, occurring mostly at night. There was no clear relationship between the pattern of GH secretion and the phase of the oestrous cycle in rats continuously sampled over a 5-day period. In ovariectomized rats, the day:night difference was maintained, though the nocturnal GH surges were larger and of longer duration than in intact females. Male rats produced multicomponent GH bursts which continued unchanged throughout the day and night. This study shows for the first time that female rats switch to a rapid, highly pulsatile pattern of GH release at night, which can only be resolved by rapid blood sampling over extended periods in conscious undisturbed animals.

J. Endocr. (1987) 114, 399–407
The dynamics of LH-induced desensitization of adenylate cyclase and LH receptor internalization in rat Leydig cells at physiological levels of LH
Authors: Habberfield A. D. , Dix C. J. , Cooke B. A.
Published: December 2008

The LH-induced desensitization of adenylate cyclase and LH receptor internalization in rat Leydig cells in vitro has been investigated using sub-physiological to pharmacological concentrations of LH.

Leydig cells pretreated with LH for 1 h in the presence of a phosphodiesterase inhibitor showed a dose-dependent decrease in the subsequent response to a high dose of LH; this was significant with concentrations of > 350 fmol/l. The maximum amount of desensitization was 60%.

The time-course of LH-induced desensitization of the adenylate cyclase system was investigated; with 3 nmol LH/1 cyclic AMP was increased in a linear manner up to 45 min, after which time there was either no further production or (with the higher concentrations) a decreased rate of production. In order to determine whether the 'non-desensitized' adenylate cyclase activity was dependent upon LH, the LH-treated cells were acid-washed to remove residual LH; cyclic AMP production still continued, albeit at a lower rate, thus indicating that this adenylate cyclase activity did not require the further presence of LH. The effect of various concentrations of LH on the level of surface-associated LH receptors was determined in the presence of monensin to prevent receptor recycling. A dose- and time-dependent decrease was found; this was significant after 2 h with 3·5 pmol LH/1 and reached a maximum of 63% of the control with 3·5 nmol/l. A dose- and time-dependent reversal of desensitization occurred if the cells pretreated with LH were washed and reincubated; with 35 pmol LH/1 and after 2 h the cells were fully responsive to a challenge with fresh LH. With higher concentrations of LH in the pretreatment, partial or no recovery was found.

These studies demonstrate that physiological and sub-physiological concentrations of LH induce a rapid desensitization of Leydig cell adenylate cyclase. Internalization of occupied and unoccupied LH receptors also occurred. It is proposed that these two events are linked and may, paradoxically, and because of the low numbers of LH receptors, be necessary to maintain the normal response of Leydig cells to LH in vivo.

J. Endocr. (1987) 114,415–422
Effect of adrenalectomy on LH release in sheep during the anoestrous season
Authors: Montgomery G. W. , Martin G. B. , Locatelli A. , Pelletier J.
Published: December 2008

An experiment was conducted to measure LH pulse frequencies in bilaterally adrenalectomized Ile-de-France ewes during the mid-anoestrous season. Seven ewes were adrenalectomized under general anaesthesia and maintained on daily injections of 3 mg deoxycorticosterone acetate (DOCA). Adrenalectomy did not affect the patterns of LH release and the mean intervals between pulses in the adrenalectomized and sham-operated control ewes were 48 and 52 min respectively. Small implants of oestradiol significantly reduced the frequency of LH pulses in both groups and, in the presence of oestradiol, there were no differences in LH release between adrenalectomized and sham-operated ewes, with the mean interpulse intervals being 91 and 89 min respectively. In a second experiment, designed to assess the effects of DOCA on LH release, the mean interpulse intervals in unoperated control ewes (46 min) and unoperated ewes given daily injections of 3 mg DOCA (47 min) were similar to those observed in adrenalectomized and sham-operated ewes. In the presence of small implants of oestradiol, the combination of DOCA and oestradiol decreased the pulse frequency significantly more than oestradiol alone (mean interpulse intervals of 85 and 65 min respectively) suggesting that DOCA may act as a progestagen in sheep. Thus alternative treatments to DOCA for the maintenance of adrenalectomized sheep must be found for future studies on the role of adrenal steroids in the reproductive system. It appears that adrenal steroids do not play a major role in the seasonal changes in LH release in the ewe.

J. Endocr. (1987) 114,437–442
IMMUNIZATION AGAINST AN INHIBIN SUBUNIT PRODUCED BY RECOMBINANT DNA TECHNIQUES RESULTS IN INCREASED OVULATION RATE IN SHEEP
Authors: Forage R.G. , Brown R.W. , Oliver K.J. , Atrache B.T. , Devine P.L. , Hudson G.C. , Goss N.H. , Bertram K.C. , Tolstoshev P. , Robertson D.M. , de Kretser D.M. , Doughton B. , Burger H.G. , Findlay J.K.
Published: December 2008

Seven Merino–Border Leicester cross–bred ewes were immunized with a purified fusion protein, produced by recombinant DNA methods, of the a subunit of bovine inhibin. Four animals were immunized with the fusion protein alone and three with a conjugate made by coupling the fusion protein to keyhole limpet haemocyanin (KLH) using glutaraldehyde. Each animal received four injections of the fusion protein over 93 days. The animals were synchronized using progestagen sponges and subjected to laparoscopy for the determination of ovulation rates in two consecutive cycles (days 115 and 135). The immunized animals had overall mean ovulation rates for each cycle of 3.4 and 3.4 which was significantly (P < 0.001) above the rates of 1.1 and 1.4 determined for the controls, which had either received no treatment (n=5) or had been immunized with 300 μg KLH (n=4). Analysis of antisera taken on day 115 showed significant fusion protein antibodies and iodinated inhibin–binding capacity in the test but not control groups. Furthermore, antisera to the fusion protein in four out of seven ewes neutralized the inhibin bioactivity of ovine follicular fluid in an in–vitro bioassay. These data demonstrate that neutralization of inhibin can be effected by immunization with bovine inhibin a subunit and that such immunization results in increased ovulation rates as predicted from the biological role of inhibin as a suppressor of FSH.
In-vitro evidence for the autoregulation of prolactin secretion at the level of the pituitary gland in the rat
Authors: Bentley A. M. , Wallis M.
Published: December 2008

The autoregulation of rat prolactin secretion at the level of the pituitary gland was investigated, using a static incubation system. The rate of prolactin secretion from the female anterior pituitary gland in vitro was found to be constant when the medium was changed at 20-min intervals. However, when the medium was left unchanged and secretory products were allowed to accumulate, prolactin secretion began to decline within 60 min. This effect was not observed with the male tissue, where the level of accumulated prolactin did not reach that at which the inhibition occurred using female tissue.

The nature of the putative secretory product causing the inhibition of prolactin secretion was investigated. Exogenous bovine prolactin (1–4 mg/l) caused an inhibition of endogenous rat prolactin secretion. Inclusion of monoamine oxidase in unchanged medium, to prevent dopamine accumulation in the medium (a possible consequence of co-storage and cosecretion with prolactin granules), did not prevent the inhibition observed in the control incubation. We therefore conclude that in-vitro autoregulation of prolactin secretion can occur at the level of the pituitary gland, probably due to the accumulated prolactin having a feedback action on the lactotroph. This might be of physiological significance if localized concentrations of the hormone within the gland are high.

J. Endocr. (1987) 115, 13–18
Effect of oestradiol-17β on perineal and neck skin glands in heifer calves
Authors: Blazquez N. B. , Long S. E. , Perry G. C. , Watson E. D.
Published: December 2008

Ten 16-week-old Friesian × Hereford heifer calves were split into experimental and control groups. Experimental animals were given an implant of oestradiol-17β in the ear whilst controls were given blank implants. They were killed 14 days later. After implantation the experimental group had consistently greater (P<0·01) plasma concentrations of oestradiol-17β than the control group. After death, sebaceous gland volume in the perineal region was greater (P < 0·01) in the experimental than in the control group, whereas sebaceous gland volume in the neck was smaller (P <0·01). Sweat gland volume in the perineal region was greater (P<0·01) in the experimental than in the control group. There was no difference between groups in the volume of sweat glands in the neck.

J. Endocr. (1987) 115, 43–46
Modulation by oestrogen of thyroid hormone effects on thyrotrophin gene expression
Authors: Franklyn J. A. , Wood D. F. , Balfour N. J. , Ramsden D. B. , Docherty K. , Sheppard M. C.
Published: December 2008

The role of oestrogen in the regulation of TSH gene expression is unclear. We have examined the effect of administration of oestrogen in the rat on serum TSH, pituitary TSH content and pituitary cytoplasmic concentrations of mRNA encoding the TSH β and α subunits, thus deriving measures of hormone release and synthesis. In addition, we have examined the effect of oestrogen on the binding of tri-iodothyronine (T3) to nuclear receptors in the anterior pituitary.

Administration of oestrogen did not affect serum concentrations of TSH in euthyroid or untreated hypothyroid rats, but did augment the effects of T3 (1 and 2 μg on serum TSH in hypothyroid animals 6 h after injection of T3. No influence of oestrogen or of thyroid status on pituitary content of TSH was seen.

A marked increase in the concentrations of TSH β and α mRNA in pituitary cytoplasm was found in hypothyroidism, compared with those in the euthyroid state. No effect of oestrogen on TSH mRNA was seen in euthyroid animals but concentrations of TSH β and α mRNA were lower in hypothyroid animals than in vehicle-treated controls. A stimulatory influence of T3 on TSH mRNA was seen 6 h after injection of T3; this stimulation was absent in oestrogen-treated rats. No effect of oestrogen on the action of T3 was evident 72 h after beginning treatment with T3. In addition to effects on serum TSH and TSH mRNA, an increase in the number of pituitary nuclear receptors for T3 was seen after oestrogen treatment.

The influences of oestrogen on serum TSH and on TSH mRNA are consistent with augmentation of thyroid hormone effects; this influence may be mediated by an increase in the number of pituitary nuclear receptors for T3.

J. Endocr. (1987) 115, 53–59
ACTH and adrenal aerobic glycolysis. II: Effects of aminoterminal peptide fragments on lactic acid and steroid production by mouse adrenocortical cells
Authors: Hinson J. , Birmingham M. K.
Published: December 2008

The effects of shortening the ACTH molecule from either end of the peptide chain on adrenal glycolysis and steroidogenesis were examined in mouse adrenal cell suspensions. Shortening the (1–24) sequence to (1–17), (1–16) and (1–14), thereby interfering with the basic tetrapeptide (15–18) assigned to the address message, progressively reduced both glycolytic and steroidogenic potencies by four, six and ten orders of magnitude respectively, without impairing the capacity for maximal excitation. The glycolytic potency of the (1–18) sequence, which was amidated at the C-terminal, equalled that of ACTH(1–24), but the steroidogenic potency was reduced by an order of magnitude. The (1–13) sequence of α-MSH, which contains substitutions at both terminals, had glycolytic and steroidogenic potencies intermediate between those of ACTH(1–16) and ACTH(1–17). Deletion of Ser1,Tyr2 from ACTH(1–18)-NH2 reduced both potencies by an order of magnitude. ACTH(11–24) and (7–38) were inactive or inhibitory.

The capacity for excitation was further examined by comparing responses to peptide fragments (1–4), (1–10), (1–13), (4–10), (4–11), (5–10), (5–14), (7–13) and (11–24) at a concentration of 1 mmol/l. All fragments, excepting (1–4), (5–10) and (11–24) were active. The activities of fragments (5–14) and (7–13), as opposed to (5–10), suggest that the requirements for methionine in position 4 may be replaced by the (11–13) tripeptide. The relative glycolytic responses of fragments containing the (11–13) sequence exceeded the steroidogenic responses, suggesting that the (11– 13) sequence may be specifically implicated in a receptor involved in glycolysis. With this exception, the functional domains within the ACTH molecule responsible for excitation, potentiation and affinity appear to be in similar locations for both evocation of glycolysis and steroidogenesis, judging from the parallel responses to reduction in chain length.

J. Endocr. (1987) 115, 71–76
Sexual activity increases plasma concentrations of cholecystokinin octapeptide and offsets hunger in male rats
Authors: Linden A. , Hansen S. , Bednar I. , Forsberg G. , Södersten P. , Uvnäs-Moberg K.
Published: December 2008

Male rats deprived of food for 48 h ignored food pellets immediately after ejaculating with a sexually receptive female rat as did males tested 5 min after i.p. injection of 5 μg cholecystokinin octapeptide (CCK-8) or males which had consumed food pellets for 1 h. The concentration of CCK-8 in plasma was increased to comparable levels (10·1±3·8 (s.e.m.); 11·3 ± 3·7 and 7·2± 0·5 pmol/l respectively, compared with 1·2 ± 0·3 pmol/l for NaCl-injected controls) under each of these conditions, whereas the concentration of gastrin increased only after food consumption (18·4 ± 3·8; 17·7 ± 5·4 and 54·3± 7·0 pmol/l respectively, compared with 21·5 ± 2·1 pmol/l for NaCl-injected controls). The effect of ejaculation on the latency to starting to eat was partially reversed by i.p. injection of 50 mg of the CCK-8 antagonist proglumide, but neither treatment with proglumide or CCK-8 nor consumption of food affected the display of sexual behaviour. The results support the suggestion that CCK-8 is a 'satiety peptide' in the rat.

J. Endocr. (1987) 115, 91–95
Effect of 1,25-dihydroxyvitamin D3 on plasma concentrations of calcium-binding protein in normal and rachitic (vitamin D-dependent rickets type I) pigs
Authors: Maunder E. M. W. , Pillay A. V. , Care A. D.
Published: December 2008

An i.v. injection of calcitriol (1,25-(OH)2D3) had no effect within 2·5 h on plasma concentrations of calbindin-D9k (vitamin D-induced calcium-binding protein; CaBP) in hypocalcaemic pigs with inherited vitamin D-dependent rickets type I or in their normocalcaemic siblings or half-siblings. Three days later the plasma concentration of CaBP had doubled in the hypocalcaemic pigs, but was unaltered in the normocalcaemic siblings and half-siblings. Following daily i.v. injections of 1,25-(OH)2D3 for a further 5 days (days 4–8) plasma concentrations of CaBP increased in both the hypocalcaemic (days 4–8) and normocalcaemic (day 8) pigs, the effect being more rapid and greater in the hypocalcaemic 1,25-(OH)2D3-deficient animals. An i.v. injection of 1,25-(OH)2D3 to pure Yucatan pigs also had no effect on plasma concentrations of CaBP within 1·5 h, but in the following 1 h there was some indication of an increase in plasma CaBP levels.

In contrast to the normal pigs, insulin-induced hypoglycaemia did not lead to a peak in plasma CaBP concentrations in the hypocalcaemic pigs. There was also no change in the plasma concentrations of 1,25-(OH)2D3 associated with the peak in plasma CaBP following insulin-induced hypoglycaemia in normocalcaemic pigs. These results suggest that changes in plasma concentrations of 1,25-(OH)2D3 are not directly involved in mediating the increase in plasma CaBP which follows hypoglycaemia induced by insulin in normal pigs, although 1,25-(OH)2D3 probably plays a permissive role.

J. Endocr. (1987) 115, 129–134
Growth hormone induction of insulin-like growth factor I messenger RNA in primary cultures of rat liver cells
Authors: Norstedt G. , Möller C.
Published: December 2008

Primary liver cells from adult rats were used to study the hormonal regulation of mRNA coding for insulin-like growth factor I (IGF-I). IGF-I mRNA could be detected at a low concentration in liver cells prepared from hypophysectomized rats and cultivated for 3 days. When these cells were exposed to GH on the second day, a dose-dependent increase in IGF-I mRNA was observed. The continuous presence of serum was not a prerequisite for this response, since GH also induced IGF-I mRNA in a defined hormone-supplemented medium. It is concluded that GH can induce IGF-I mRNA in the liver by a direct mechanism.

J. Endocr. (1987) 115, 135–139
Modulation by continuous oestrogen treatment and by progesterone of oestrogen receptors in the rabbit uterus
Authors: Batra S. , Owman Ch. , Rydhström H. , Sjöberg N.-O.
Published: December 2008

The effect of continuous oestrogen treatment on uterine weight, and on cytoplasmic and nuclear oestrogen receptors was examined in rabbits. Modulation of the effects of oestrogen by progesterone was also studied. Uterine weight increased successively after exposure to oestrogen from 1 to 6 days. The concentration of both cytosolic and nuclear oestrogen receptors decreased in almost parallel fashion, however, irrespective of whether it was expressed per μg protein or μg DNA. Treatment with progesterone 5 days after oestrogenization caused no significant change in uterine weight at first. The oestrogen receptor concentration in both cytosolic and nuclear fractions decreased after 1 day but increased again after 3 days of progesterone treatment. The results indicated that there is a reduction in the actual concentration of oestrogen receptors in both cytosolic and nuclear fractions after continuous oestrogen treatment. The antagonism by progesterone of the effects produced by oestrogen appears to be transitory in nature, at least in the rabbit uterus.

J. Endocr. (1987) 115, 199–203
Effect of low temperatures on glucose-induced insulin secretion and ionic fluxes in rat pancreatic islets
Authors: Escolar J. C. , Hoo-Paris R. , Castex Ch. , Sutter B. Ch. J.
Published: December 2008

The direct effect of cold on the inhibition of B cell secretion is well known in hibernating and experimentally hypothermic mammals. This temperature dependency may result from the inhibition of ion transport across the membranes. In order to verify this hypothesis, ionic effluxes and insulin secretion from rat islets loaded with 86Rb+ and 45Ca2+ were measured during perifusion.

At 37 °C, the rise in glucose concentration from zero to 16·7 mmol/l provoked a rapid decrease in 86Rb+ efflux, an early fall and subsequent rise in 45Ca2+ efflux and a typical biphasic pattern of insulin secretion. At 27 °C, glucose induced only a very slight increase in insulin secretion, while the fluxes of radioactive ions were not significantly modified in amplitude but were clearly delayed. At 17 °C, no insulin response to glucose was observed and the decrease in K+ conductance indicated by 86Rb+ flux decrease was less temperature-dependent than the movement of Ca2+. After supplementary stimulation with a high extracellular concentration of Ca2+, insulin secretion was enhanced at 27 °C and reached levels induced by glucose alone at 37 °C. An increase in hormone secretion occurred even at 17 °C, but only during a first phase of secretion.

Regular increases in temperature potentiated insulin secretion and provoked changes in ionic fluxes which suggest that B cell depolarization (86Rb+ flux decrease) induced by glucose can occur at 15 °C but cannot induce the opening of voltage-dependent Ca2+ channels (increase in 45Ca2+ efflux) until temperatures higher than 27 °C are reached.

These results suggest that cooling affects calcium movements especially rather than K+ conductance and insulin exocytosis per se.

J. Endocr. (1987) 115, 225–231
Effect of thyroid hormones on angiotensinogen production in the rat in vivo and in vitro
Authors: Ruiz M. , Montiel M. , Jimenez E. , Morell M.
Published: December 2008

The influence of thyroid hormones on angiotensinogen production was studied in vitro and in vivo. In the in-vitro system, angiotensinogen production rate (APR) of monolayer cultures of rat hepatocytes in response to tri-iodothyronine (T3) and thyroxine (T4) was assayed. In the in-vivo system, plasma angiotensinogen concentration (PAC) and liver angiotensinogen content (LAC) were measured in hyper- and hypothyroid rats. In both thyroid dysfunctions, a significant decrease of PAC was found compared with that in control animals; however, LAC showed a significant increase in hyperthyroidism and a marked decrease in hypothyroidism. As PAC is dependent upon both angiotensinogen production by the liver and angiotensinogen degradation by renin, the decrease in PAC observed in hyperthyroidism could be due to an increase in plasma renin concentration, which would overcome the increased synthesis of liver angiotensinogen observed in these animals. In fact, addition of various concentrations of T4 or T3 to monolayer cultures of adult rat hepatocytes significantly enhanced APR. This increase was greater and started earlier with T3 (1196·1 ± 143·7 (s.d.) pg/mg protein per 6-h incubation; significant differences at the third hour of incubation) than with T4 (858·3 ± 88·2 pg/mg protein per 6-h incubation; significant differences at the sixth hour of incubation). In addition, a close dose–response relationship was found in the cultures supplemented with T3. The different time-course in the response elicited by T3 and T4 on APR could be a consequence of the necessary transformation of T4 into T3 to acquire biological activity.

J. Endocr. (1987) 115, 311–315
Renal vasopressin receptors in ageing C57BL/Icrfat mice
Authors: Davidson Y. S. , Davies I. , Goddard C.
Published: December 2008

The mechanism of water conservation is impaired in ageing mammals. An age-related defect in the release of vasopressin has been implicated but, more recently, attention has moved to the renal component of the water conservation mechanism. Previous studies using renal cells prepared from mice of different ages have shown that the threshold dose of vasopressin required to elicit a significant rise in cyclic AMP (cAMP) was greater in older animals. The dose–response curve was moved to the right in 35-month-old mice, i.e. the concentration of vasopressin required to give maximum cAMP output was increased. To investigate this further we examined the binding of vasopressin to renal medullary cells maintained in short-term culture, to determine whether the decreased response of cAMP levels to vasopressin is due to changes in hormone-receptor interaction. In 6-month-old male mice the dissociation constant (Kd) was 2·38 nmol/l and the maximum binding of the hormone (Bmax) was 47·6 fmol/106 cells, and at 30 months of age Kd was 2·37 nmol/l and Bmax was 47·0 fmol/106 cells. In female mice the changes were more complicated because the data for the 6-month-old mice could be split into two groups. It is concluded that there are no age-related differences in the numbers of receptors or their affinity for vasopressin, and that the decreased cAMP response is probably associated with post-receptor mechanisms in this species.

J. Endocr. (1987) 115, 379–385
A direct action of human calcitonin gene-related peptide on isolated osteoclasts
Authors: Zaidi M. , Chambers T. J. , Das R. E. Gaines , Morris H. R. , MacIntyre I.
Published: December 2008

The calcitonin gene encodes a small family of peptides: calcitonin, calcitonin gene-related peptide (CGRP) and katacalcin. Whereas calcitonin is concerned with skeletal maintenance, the function, if any, of katacalcin is still unknown. In the present study we have assessed resorption of human cortical bone substrate by isolated rat osteoclasts and have shown that CGRP acts directly on the osteoclast to inhibit bone resorption. The three CGRP peptides (rat, human(a) and human(β)) caused an almost equivalent decrease in osteoclastic bone resorption and were approximately 1000-fold less potent than human calcitonin in this respect. The responses of human calcitonin and human CGRP(α) were additive. Furthermore, prior treatment with trypsin to destroy receptors abolished the responsiveness of osteoclasts to CGRP and calcitonin. The carboxyl- and amino-terminal fragments of CGRP were found not to inhibit bone resorption, suggesting that the whole molecule of CGRP is necessary for biological activity. We have therefore suggested that the calcitonin-like effects of CGRP, seen both in vivo in the rat bioassay and in vitro in organ cultures, are due to the direct action of CGRP on the osteoclast, probably mediated through the calcitonin receptor. Though it is unlikely that CGRP is involved in the regulation of plasma calcium, the peptide may be an important local regulator of bone cell function.

J. Endocr. (1987) 115,511–518
Identification of multiple low molecular weight placental prolactin-like proteins produced by rat trophoblast cells
Authors: Soares M. J. , De S. K. , Foster B. A. , Julian J. A. , Glasser S. R.
Published: December 2008

Rat trophoblast tissue was found to synthesize a number of low molecular weight proteins possessing prolactin-like characteristics. There appear to be at least three proteins that cross-react with antisera to pituitary prolactin. Two of the proteins had a molecular weight of 25 000, similar to ovine pituitary prolactin, and isoelectric points of 6·8 and 7·0. The third immunoreactive protein had a lower molecular weight (23 500), similar in size to human placental lactogen, and a slightly more acidic isoelectric point of 6·75. The molecular weight variants cross-reacted with an antipeptide serum that was generated to a synthetic peptide representing amino acids 150 to 164 of rat placental lactogen-2 (PL-2). Based on this analysis, we consider these proteins to be related to PL-2.Analysis of trophoblast proteins by gel-filtration chromatography resulted in the identification of another trophoblast prolactin. This material eluted earlier than PL-2-related proteins on a gel-filtration column, possessed prolactin-like activity (determined by competition with ovine pituitary prolactin for rabbit mammary gland or rat liver prolactin receptors) but showed limited cross-reactivity with either the antiserum to pituitary prolactin or the antiserum to the PL-2 peptide. We have thus identified multiple low molecular weight trophoblast prolactins, possessing different biochemical and immunological characteristics.

J. Endocr. (1988) 116, 101–106