bluuebunny/crossref_metadata_2025_split huggingface dataset:
Atrial natriuretic factor inhibits the stimulated in-vivo and in-vitro release of vasopressin and oxytocin in the rat
Authors: Poole C. J. M. , Carter D. A. , Vallejo M. , Lightman S. L. 
Published: December 2008

ABSTRACT
The effect of an atrial natriuretic peptide on the secretion of the neurohypophysial peptides arginine vasopressin (AVP) and oxytocin has been studied in vivo and in vitro. Atriopeptin III was administered intracerebroventricularly to conscious rats and plasma concentrations of AVP and oxytocin were determined both in controls and in rats which had their drinking water replaced by 2% NaCl. The release of both AVP and oxytocin was inhibited when basal levels were increased by the saline treatment. The inhibition of AVP release lasted for 40 min whereas oxytocin release was inhibited for 10 min only. In a further experiment the stimulated release of AVP and oxytocin from the isolated neurointermediate lobe of the rat was also inhibited by atriopeptin III.
J. Endocr. (1987) 112, 97–102
Inhibition of testosterone metabolism in the brain and cloacal gland of the quail by specific inhibitors and antihormones
Authors: Alexandre C. , Balthazart J. 
Published: December 2008

ABSTRACT
The effects of antioestrogens, antiandrogens and of various inhibitors of testosterone metabolism on testosterone metabolism in the quail hypothalamus and cloacal gland were studied by an in-vitro radio-enzymatic assay. It was found that antioestrogens and antiandrogens generally had little or no effect on aromatase and 5α- and 5β-reductases of testosterone, except when used at very high doses. The 5α-reductase inhibitor, 17β-N,N-diethylcarbamoyl-4-methyl-4-aza-5α-androstan-3-one, inhibited both 5α- and 5β-dihydrotestosterone production without markedly affecting aromatase activity. Surprisingly, the aromatase inhibitor, 1,4,6-androstatriene-3,17-dione, inhibited not only the production of oestradiol but also that of 5β-dihydrotestosterone and, to a lesser extent, 5α-dihydrotestosterone. These unexpected properties should be taken into account when interpreting the results of in-vivo experiments using these compounds.
J. Endocr. (1987) 112, 189–195
Sodium transport and the cellular sodium transport pool of colonic epithelium: effects of sodium loading, aldosterone and lithium
Authors: Edmonds C. J. , Mackenzie J. 
Published: December 2008

ABSTRACT
The cellular sodium transport pool and sodium transepithelial fluxes were investigated in vivo in rat distal colon in relation to sodium loading by intravenous infusion (3·5 h), and to short (4 h) and prolonged (72 h) i.v. administration of aldosterone. Considerable natriuresis and increase in body sodium content were produced by the sodium load but there was no significant effect on the transcellular sodium flux (active absorption from lumen to plasma) or on the sodium transport pool. Both short and prolonged aldosteronism produced similar increases in the transport pool and in the transcellular sodium flux, but the transepithelial electrical potential difference (p.d.) was significantly greater in rats given the prolonged infusion. Addition of amiloride to the solution in the lumen of the colon almost completely abolished the p.d., the transport pool and the transcellular sodium flux of the rats receiving prolonged infusion, but had much less effect in those given the short infusion. The time-course of recovery of p.d. following prolonged aldosteronism was similar to that described for the turnover rate of rat colonic epithelial cells.
Lithium within the lumen had no significant effect in untreated rats but after prolonged aldosterone infusion lithium reduced the p.d. and the transcellular sodium flux although the transport pool was not reduced. These findings are consistent with the hypothesis that aldosteronism renders the apical membranes of the epithelial cells permeable to lithium and that intracellular accumulation of lithium depresses active sodium transfer.
The observations are interpreted in terms of an epithelial model in which aldosterone induces amiloride-sensitive pathways (diffusion channels permeable to sodium and lithium) in the apical membrane which totally replace the amiloride-insensitive pathways when aldosteronism is prolonged; the resulting expansion of the sodium transport pool is the stimulus for increased active sodium transport across the basolateral membranes.
J. Endocr. (1987) 112, 247–252
Adrenal synthesis of corticosterone in response to ACTH in rats is influenced by leukotriene A4 and by lipoxygenase intermediates
Authors: Jones D. B. , Marante D. , Williams B. C. , Edwards C. R. W. 
Published: December 2008

ABSTRACT
The possible involvement of the lipoxygenase pathway of arachidonic acid metabolism in the events which take place during ACTH-induced stimulation of corticosterone secretion has been studied using an isolated rat adrenal cell system. Incubation with arachidonic acid resulted in an inhibition of ACTH-stimulated corticosterone production. The lipoxygenase pathway inhibitors nordihydroguaretic acid (NDGA), eicosatetraynoic acid (ETYA) and compound BW755C also produced inhibition of ACTH-stimulated corticosterone synthesis. The concentrations of the inhibitors at which 50% inhibition occurred were 15, 34 and 37 μmol/l respectively. The inhibitions produced by NDGA and ETYA were independent of cyclic AMP output. NDGA also inhibited corticosterone production induced by dibutyryl cyclic AMP but had no effect on corticosterone synthesis induced by pregnenolone.
Preincubation of adrenal cells with the lipoxygenase products 5, 12 and 15 hydroxyeicosatetraenoic acid (HETE) and with leukotrienes A4, B4, C4, D4 and E4 resulted in significant inhibitions of corticosterone production in response to ACTH with leukotriene A4 (LTA4) and with 15HETE and 5HETE. Conversely, incubation with glutathione (GSH), which is known to reduce intracellular LTA4 levels, produced stimulation (at 5 mmol GSH/1) and inhibition (at 50 mmol GSH/1) of corticosterone output. These studies suggest that the lipoxygenase pathway may be involved in ACTH-stimulated corticosterone synthesis.
J. Endocr. (1987) 112, 253–258
Role of protein kinase C in the pigment cell of the lizard (Anolis carolinensis)
Authors: Lucas A. M. , Thody A. J. , Shuster S. 
Published: December 2008

ABSTRACT
The role of protein kinase C in melanosome dispersion was examined using the melanophores of the lizard Anolis carolinensis and an in-vitro rate method of bioassay. The phorbol ester 12-O-tetradecanoyl-phorbol-13-acetate (TPA), which directly activates protein kinase C, was able to potentiate the melanophore response to α-MSH in a dose-dependent manner. Similarly, the stimulatory response to forskolin, which activates the adenylate cyclase catalytic subunit, was also potentiated by TPA. The response of the melanophore to cyclic AMP, however, remained unaltered by any dose of TPA. We thus propose that the potentiation of α-MSH potency by TPA is through an interaction of protein kinase C with adenylate cyclase and, more specifically, that this interaction may be at the level of the linkage of the nucleotide regulatory subunit Ns with the catalytic moiety C of adenylate cyclase.
J. Endocr. (1987) 112, 283–287
Extraction and characterization of a cytochemically assayable Na+/K+-ATPase inhibitor/glucose-6-phosphate dehydrogenase stimulator in the hypothalamus and plasma of man and the rat
Authors: Millett J. A. , Holland S. M. , Alaghband-Zadeh J. , de Wardener H. E. 
Published: December 2008

ABSTRACT
Some physicochemical properties of partially purified hypothalamic material from the spontaneously hypertensive rat, and of plasma from man and the rat, have been characterized using a validated cytochemical bioassay which measures the ability of biological fluids to stimulate fresh guinea-pig kidney glucose-6-phosphate dehydrogenase (G6PD) after 2 min of exposure to the test substance, as an indication of their ability to inhibit Na+/K+ adenosine triphosphatase (Na+/K+-ATPase) after 4–6 min of exposure.
The G6PD-stimulating activity of both hypothalamic extract and plasma is soluble in water and insoluble in chloroform. During electrophoresis the activity from both sites appears in the same fractions and travels considerably further than lysine. After high-pressure liquid chromatography the activity of hypothalamic extract appears in a discreet fraction which does not absorb u.v. light. The activity of both the hypothalamic extract and plasma survives boiling and acid hydrolysis, but is substantially inhibited by prior incubation with digoxin antibody. From ultrafiltration studies, the substance responsible for the ability to stimulate G6PD appears to have a molecular weight of less than 500. The G6PD-stimulating activity of hypothalamic extracts was destroyed by ashing and by base hydrolysis. The ability of plasma of high activity to stimulate G6PD is considerably increased by incubating at 37 °C for 15 min and destroyed by incubation for 45 min.
It is concluded that these and several other previously noted similarities suggest that the cytochemically assayable Na+/K+-ATPase-inhibiting/G6PD-stimulating activity in the plasma and hypothalamus may be due to the same ouabain-like substance.
J. Endocr. (1987) 112, 299–303
Indomethacin treatment prevents prolactin-induced luteolysis in the rat
Authors: Sánchez-Criado J. E. , Ochiai K. , Rothchild I. 
Published: December 2008

ABSTRACT
Adult female rats were hypophysectomized and their pituitary glands autotransplanted beneath the left kidney capsule on day 2 (day 1 was the day of ovulation). In such rats the pituitary secretes prolactin fairly constantly and the corpora lutea secrete progesterone for several months. To induce the luteolytic effect of prolactin the rats were first injected s.c. with 2-bromo-α-ergocryptine (CB-154) on cycle days 12, 13 and 14 (i.e. 10, 11 and 12 days after operation) to depress prolactin secretion, and then with CB-154 vehicle (70% ethanol) daily until cycle day 21, to allow prolactin secretion to resume. One ovary was removed from each rat on day 15 and the remaining one on day 22. The mean (± s.e.m.) weight of the corpora lutea on day 15 was 1·46±0·06 mg and 0·98±0·07 mg on day 22 (n = 17). In contrast, rats in which the CB-154 treatment was maintained to day 21 had corpora lutea which weighed 1·31 ±0·09 on day 15 and 1·47 ±0·08 mg on day 22 (n = 15). To investigate whether indomethacin, a prostaglandin synthesis inhibitor, affected the luteolytic action of prolactin, the experiment was repeated, but on day 15 (after the removal of one ovary) the groups in which CB-154 treatment was stopped, as well as the group in which CB-154 treatment was maintained, were each divided into two groups. In one, indomethacin-containing silicone elastomer wafers and, in the other, blank silicone elastomer wafers, were placed within the bursa of the remaining ovary. There were no differences in corpus luteum weight on day 15 among any of these groups and the two groups of the first experiment.
There was no significant difference in corpus luteum weight between day 15 and day 22 in any of the six groups except for the two groups treated with the CB-154 vehicle and not with indomethacin. Thus, treatment with indomethacin prevented the fall in corpus luteum weight associated with the discontinuation of CB-154 treatment.
Serum prolactin levels fell until day 15 in all rats and remained low in those in which the CB-154 treatment was maintained to day 21, but returned to control values in those treated with vehicle after day 14. Serum progesterone levels fell and remained low in all groups. Indomethacin treatment had no effect on the levels of either serum prolactin or progesterone. We conclude that some of the pharmacological effects of indomethacin are to prevent prolactin-induced luteolysis, and we suggest that prolactin induces rapid regression of the corpus luteum by stimulating intraluteal prostaglandin production or by being necessary for the effect of luteolytic prostaglandins.
J. Endocr. (1987) 112, 317–322
A quantitative study of steroid bioconversions in the testis of the African catfish, Clarias gariepinus (Burchell), under natural spawning and natural and cultivated non-spawning conditions
Authors: Schoonen W. G. E. J. , Lambert J. G. D. , Resink J. W. , Viveen W. J. A. R. , Van Oordt P. G. W. J. 
Published: December 2008

ABSTRACT
Quantitative aspects of bioconversions in the testes of the African catfish (Clarias gariepinus) were studied in vitro by incubation of tissue with [3H]pregnenolone or [3H]androstenedione. During the breeding period, spawning and non-spawning animals were collected from their natural habitat, the Hula nature reserve, in northern Israel. In the same period, non-spawning animals were collected from a fish pond in the same region. It was shown that spawning was accompanied by significant changes in steroid bioconversions, i.e. a reduction in androgen synthesis, especially of 11β-hydroxyandrostenedione and 11β-hydroxytestosterone and an increase in the production of C21-steroids, especially progesterone, 17α-hydroxyprogesterone and a pregnenolone ester. These changes resulted from a decreased contribution of the cytochrome P-450 enzymes 17α-hydroxylase, C17–20-lyase and 11β-hydroxylase. A rise in plasma gonadotrophin concentration was observed only in spawning catfish. In the absence of such an increase in plasma gonadotrophin, steroid synthesis in the testes of non-spawning feral and pond catfish was primarily directed towards the production of 11-oxygenated androgens and 5β-pregnane-3α,17α,20α-triol. It is suggested that spawning is induced by gonadotrophin and the ensuing change in steroidogenesis. It is possible that husbandry conditions inhibit the necessary increase in gonadotrophin release.
J. Endocr. (1987) 112, 323–332
Comparison of the cellular composition and steroidogenic properties of preparations of interstitial cells isolated from immature and mature rat testis
Authors: Themmen A. P. N. , Molenaar R. , Visser W. J. , Jongkind J. F. , Rommerts F. F. G. , van der Molen H. J. 
Published: December 2008

ABSTRACT
The morphological and steroidogenic properties of preparations of interstitial cells isolated by collagenase treatment from testes of immature and mature rats have been compared.
After additional purification on a Ficoll gradient, 80% of cells from mature rat testes were found to be Leydig cells; 20% were macrophages. Forty to sixty per cent of collagenase-dispersed cells isolated from immature rats were Leydig cells, 37% were mesenchymal cells and there were no macrophages. A preparation in which 90% cells were Leydig cells could be obtained from immature testes after further purification by centrifugation through a Percoll gradient. The distribution of steroidogenic enzymes through the gradient corresponded to the distribution of LH-dependent steroid production. The results indicate that the steroidogenic activity per Leydig cell from mature rats is fourfold greater than the activity in immature rat Leydig cells in control incubations or after stimulation with LH, dibutyryl cyclic AMP or in the presence of 22R-hydroxycholesterol.
J. Endocr. (1987) 112, 361–366
Mammary resistance: a possible controlling factor in milk ejection
Authors: Lau C. , Henning S. J. 
Published: December 2008

ABSTRACT
At 8 and 13 days post partum, rats have the same total milk availability; yet, in response to suckling they release a greater amount of milk on day 13 than on day 8. Increased sensitivity to suckling in the more advanced lactators may result from a greater release of oxytocin or from changes in the mammary glands as lactation advances. The present study explores this latter possibility in anaesthetized dams at 8–9 and 13–15 days of lactation. Milk release and intramammary pressure were measured in anaesthetized dams in response to various doses of oxytoxin. Milk release was determined from the body weight gain of pups which had been fasted for 5 h before suckling on dams which had been isolated for 5 h. This parameter was significantly greater in 13- to 15-day lactators than in 8- to 9-day lactators over the range of oxytocin doses examined. In contrast, intramammary peak pressure and its dissipation time were significantly larger in the 8- to 9-day lactators than in the 13- to 15-day lactators. The compliance of the mammary glands was indirectly assessed at the two stages of lactation. When a constant pressure pulse was introduced into a cannulated gland, the resulting pressure peak was significantly greater in 8-day than in 13-day lactators, indicating a greater resistance in the former. Taken together, these results indicate that when endogenous oxytocin is inhibited (by anaesthesia) the greater milk release observed at the later stage of lactation in response to various doses of oxytocin may be due to a decline in mammary resistance as lactation progresses.
J. Endocr. (1987) 112, 379–385
Inhibition of first ovulation: administration of an LHRH antagonist to immature female rats
Authors: Meijs-Roelofs H. M. A. , Kramer P. , van Cappellen W. A. , Schuiling G. A. 
Published: December 2008

ABSTRACT
Subcutaneous injections of an LHRH antagonist (ALHRH; Org.30093) were administered to immature female rats. Neither a single high dose (50 μg) nor repeated daily doses of 5–30 μg ALHRH/day, administered between 28 and 38 days of age, influenced the age and body weight at the time of vaginal opening or first ovulation. If repeated daily doses of 2 × 10 μg ALHRH were given from 32 to 42 or from 37 to 47 days of age, first ovulation was delayed by 3·0 and 6·3 days respectively. Administration of 10 μg ALHRH at 09.00 h and again at 17.00 h on the day of first pro-oestrus was found to be sufficient to block the expected first ovulation in 36 out of 38 rats. This effect could be repeated by administering the same doses of ALHRH at pro-oestrus and again on the next day: ovulation was blocked in eight out of eight rats. A single dose of 10 μg ALHRH, administered on the morning of pro-oestrus, blocked ovulation in five out of twelve rats. Both the preovulatory LH and FSH surge, as measured at 16.00 h on pro-oestrus, were found to be inhibited by ALHRH treatment.
On the day after pro-oestrus no recruitment of new small antral follicles had occurred in rats with ovulatory blockade. Delayed ovulation took place 2–5 days after ALHRH injection at pro-oestrus; until 3 days after injection rats were able to ovulate their original preovulatory follicles, thereafter newly developed follicles ovulated and large ovarian cysts were found in the ovaries, next to fresh corpora lutea.
Chronic administration of two injections daily of 10 μg ALHRH from 34 days of age until the morning of first pro-oestrus had marginal effects on the timing of first pro-oestrus and on follicle dynamics.
It was concluded that with the ALHRH compound used, and in chronic as well as in acute experiments, first ovulation could only be delayed by its administration on the day of first pro-oestrus and that the effect was due to acute inhibition of the preovulatory gonadotrophin surge.
J. Endocr. (1987) 112, 407–415
Antidiuretic antagonism and agonism of 1-deamino-pentamethylene-2-d-phenylalanine-4-isoleucine-arginine vasopressin in rats with diabetes insipidus
Authors: Vilhardt H. , Lundin S. 
Published: December 2008

ABSTRACT
Using implanted minipumps it was shown over a period of 7 days that the vasopressin antagonist, 1-deamino-pentamethylene-2-d-Phe-4-Ile-arginine vasopressin, caused increased diuresis in normal rats and reversed vasopressin- or oxytocin-induced antidiuresis in Brattleboro rats. When the antagonist was infused alone in Brattleboro rats it induced a marked antidiuretic response, indicating that the analogue also possessed agonistic properties. The agonist action could not be demonstrated in anaesthetized, hydrated normal rats. In these animals the analogue behaved as a pure antagonist. It is concluded that analogues which behave as antagonists in one test model may display agonistic properties under different experimental conditions.
J. Endocr. (1987) 112, 439–442
Influence of administration of ovarian steroids on the function of neutrophils isolated from the blood and uterus of ovariectomized mares
Authors: Watson E. D. , Stokes C. R. , Bourne F. J. 
Published: December 2008

ABSTRACT
The function of blood and uterine luminal neutrophils from ovariectomized mares treated with ovarian steroids was investigated 18 h after intrauterine infusion of 1 × 109 Streptococcus zooepidemicus. Random migration of blood neutrophils under agarose was reduced by treatment with progesterone compared with that of neutrophils from oestradiol-treated and control mares. In-vitro addition of progesterone to blood neutrophils from acyclic ponies also reduced migration. Uterine neutrophils did not migrate under agarose which was probably an effect of bacterial phagocytosis. Hormone treatment had little effect on phagocytosis of yeast blastospores by blood neutrophils. Phagocytosis by uterine neutrophils from oestradiol-treated and control mares was significantly better than that by blood neutrophils. In progesterone-treated mares, however, phagocytosis by uterine neutrophils was significantly lower than that in the other two treatment groups and was similar to that measured in blood neutrophils.
The results indicate a marked effect of progesterone in reducing both migration of blood neutrophils and phagocytosis by uterine neutrophils.
J. Endocr. (1987) 112, 443–448
Effects of the uterus and the ovaries on growth, somatotrophin and somatomedin A in developing rats
Authors: Biro J. C. , Eneroth P. 
Published: December 2008

ABSTRACT
The effects of hysterectomy and ovariectomy on plasma concentrations of GH, somatomedin A, TSH and thyroxine (T4) were studied in developing rats. Four groups of 24-day-old rats were ovariectomized, ovohysterectomized, hysterectomized or sham-operated. Their weights, lengths and plasma hormone concentrations were measured at 26, 43, 64, 78 and 92 days of age to investigate pre- and postpubertal differences caused by the uterus or ovaries. Plasma concentrations of the hormones examined showed a successive rise with time, but GH and somatomedin A concentrations rose mainly after the opening of the vagina (days 50–55). Higher GH and somatomedin A concentrations were found in the plasma of ovariectomized animals than in ovohysterectomized controls before puberty (GH: 260–300%, P<0·01; somatomedin A: 25–30%, P<0·05). Ovariectomized animals weighed more than ovohysterectomized females after puberty (4·5–6%, P<0·01). This indicated that the uterus exerted a stimulatory effect on GH-somatomedin A regulation and body weight gain in the absence of the ovaries.
Significantly lower plasma somatomedin A (but not GH) concentrations were found in hysterectomized and sham-operated animals than in their respective controls after puberty (30–39%, P<0·01) and their final body weight was lower (22–26%, P<0·001). There were no consecutive uterus- or ovary-related changes in plasma TSH and T4 levels.
It was concluded that both the uterus and ovaries had significant as well as opposite effects on somatomedin A and body weight with the effects of the ovaries being greater than those of the uterus.
J. Endocr. (1987) 113, 21–26