POTENTIATION BY URETHANE AND INHIBITION BY PENTOBARBITONE OF OXYTOCIN RELEASE IN VITRO

1975 ◽  
Vol 67 (3) ◽  
pp. 453-458 ◽  
Author(s):  
R. E. J. DYBALL
Keyword(s):  
Calcium Ion ◽  
Chloride Concentration ◽  
Ion Uptake ◽  
Hormone Release ◽  
Partial Explanation ◽  
Obvious Effect ◽  
Oxytocin Release ◽  
Neurotransmitter Substances ◽  
Stimulation Of

SUMMARY Isolated rat neural lobes were incubated in vitro in Locke's solution containing anaesthetic quantities of urethane, pentobarbitone or tribromoethanol. The oxytocin content of the incubation medium was estimated before, during and after stimulation of the tissue by raising the potassium chloride concentration from 5·6 to 56 mmol/l. Urethane (25 mmol/l) significantly potentiated oxytocin release (P < 0·01) whereas tribromoethanol (0·5 mmol/l) had no obvious effect and pentobarbitone (0·4 mmol/l) significantly (P < 0·01) inhibited its release. Reduction of the sodium chloride concentration in the medium potentiated the release of oxytocin in each case but did not alter its pattern. Urethane which increased secretion of oxytocin also increased calcium ion uptake by the neural lobes and pentobarbitone which decreased oxytocin release decreased calcium ion uptake. The results may explain why the blood concentration of the neurohypophysial hormones tends to be higher in rats anaesthetized with urethane than with tribromoethanol. Inhibition of hormone release by pentobarbitone suggests that this anaesthetic is unsuitable for use in studies of neurohypophysial hormone release. A partial explanation of the anaesthetic properties of urethane and pentobarbitone may also have been found if the release of neurotransmitter substances is influenced in a similar manner.

Stimulation of luteinizing hormone release by epidermal growth factor is mediated by arachidonic acid metabolism in vitro

1988 ◽  
Vol 117 (4_Suppl) ◽  
pp. S54-S55
Author(s):  
A. PRZYLIPIAK ◽  
L. KIESEL ◽  
T. RABE ◽  
K. HELM ◽  
M. PRZYLIPIAK ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Growth Factor ◽  
Luteinizing Hormone ◽  
Epidermal Growth Factor ◽  
Acid Metabolism ◽  
Arachidonic Acid Metabolism ◽  
Hormone Release ◽  
Epidermal Growth ◽  
Stimulation Of

scholarly journals Stimulus-secretion coupling in the neurohypophysis of the jerboa Jaculus orientalis.

1994 ◽  
Vol 195 (1) ◽  
pp. 19-34
Author(s):  
A Raji ◽  
J J Nordmann
Keyword(s):  
Time Course ◽  
Physiological State ◽  
Nerve Endings ◽  
Neurosecretory System ◽  
Channel Blockers ◽  
Vasopressin Release ◽  
Oxytocin Release ◽  
Stimulus Secretion Coupling ◽  
Stimulation Of

1. In many mammals, severe dehydration is known to cause exhaustion of the vasopressin content of the neural lobe. Here, we have examined the physiological state of the neurohypophysis of the jerboa Jaculus orientalis, a rodent inhabitant of a semi-desert climate. 2. Isolated neurohypophyses and neurosecretory nerve endings were perfused in vitro and vasopressin and oxytocin release were determined by radioimmunoassay. 3. Electrical stimulation of the neurohypophysis with bursts of pulses mimicking the activity of hypersecreting neuroendocrine neurones induced similar increases of secretion in both control animals and animals dehydrated for up to 2 months. Neurohormone release was greatly potentiated when the bursts of pulses were separated by silent intervals. 4. Prolonged stimulation of neurohypophyses from both control and dehydrated animals induced a sustained increase of vasopressin release; in contrast, oxytocin release under similar conditions showed a biphasic secretory pattern consisting of a transient increase that subsequently decreased to a steady level whose amplitude was similar to that for vasopressin. 5. K(+)-induced secretion was largely inhibited by the Ca2+ channel blockers nicardipine and omega-conotoxin, suggesting that in this neurosecretory system both L- and N-type calcium channels play a major role in stimulus-secretion coupling. Depolarization of isolated nerve endings using a fast-flow perifusion system showed that there was no difference in the amplitude and the time course of the secretory response in dehydrated and hydrated animals. 6. The results demonstrate that, despite the climatic conditions in which the jerboas live, their neural lobes retain the capacity to release, upon depolarization of the plasma membrane of the nerve endings, large amounts of neurohormone. It is concluded that the neurohypophyseal peptidergic release system in the dehydrated jerboa functions adequately even under extreme environmental stress.

scholarly journals Effects of benzene, quercetin, and their combination on porcine ovarian cell proliferation, apoptosis, and hormone release

2019 ◽  
Vol 62 (1) ◽  
pp. 345-351 ◽  
Author(s):  
Adam Tarko ◽  
Aneta Štochmal'ová ◽  
Katarína Jedličková ◽  
Sandra Hrabovszká ◽  
Adriana Vachanová ◽  
...  
Keyword(s):  
Granulosa Cell ◽  
Protective Action ◽  
Inhibitory Effect ◽  
Hormone Release ◽  
Ovarian Cell ◽  
Cell Functions ◽  
Ovarian Granulosa Cell ◽  
Oxytocin Release ◽  
Prostaglandin F

Abstract. We hypothesized that the environmental contaminant benzene and the plant antioxidant quercetin may affect ovarian cell functions and that quercetin could offer protection against the adverse effects of benzene. This study aimed to examine the action of benzene, quercetin, and their combination on porcine ovarian granulosa cell functions. We elucidated the effects of benzene (20 µg mL−1), quercetin (at the doses 0, 1, 10, 100 µg mL−1), and their combination on ovarian granulosa cell functions (proliferation, apoptosis, and hormone release) in vitro using immunocytochemistry and enzyme immunoassay respectively. Benzene alone stimulated proliferation, apoptosis, and oxytocin release and inhibited progesterone and prostaglandin F release. Quercetin alone inhibited proliferation, apoptosis, and stimulated oxytocin release but did not affect progesterone and prostaglandin F release. When used in combination with benzene, quercetin promoted the inhibitory effect of benzene on progesterone release. Overall, these data suggest that benzene and quercetin have direct stimulatory and inhibitory effects, respectively, on basic ovarian functions. Moreover, no protective action of quercetin against the effects of benzene was found. Rather, it was found to enhance the effect of benzene on progesterone release. Therefore, quercetin cannot be considered for preventing or mitigating the effects of benzene on reproductive processes.

Actions of somatotrophin on oxytocin and progesterone release from the microdialysed bovine corpus luteum in vitro

1994 ◽  
Vol 143 (2) ◽  
pp. 243-250 ◽  
Author(s):  
J Liebermann ◽  
D Schams
Keyword(s):  
Early Pregnancy ◽  
Oestrous Cycle ◽  
Luteal Function ◽  
Bovine Corpus Luteum ◽  
Oxytocin Release ◽  
Dose Levels ◽  
Dose Dependent ◽  
Bovine Somatotrophin ◽  
Stimulation Of

Abstract In the present investigation, the effect of recombinant (BST) and pituitary-derived (bGH) bovine somatotrophin on progesterone and oxytocin release was examined. Individual copora lutea (CL) were obtained from cows at different stages of the oestrous cycle (days 5–7, 8–12 and 15–18) and also from early pregnancy (days 60–120) and were implanted with an in vitro microdialysis system (MDS). Perfusion with BST for 60 min (005, 0·5 and 5 μmol/l) induced a dose-dependent stimulation of progesterone release. Release of oxytocin from CL was significantly stimulated by BST at all dose levels. BST (0·5 μmol/l) stimulated progesterone release most during the early and mid-luteal phases and oxytocin release especially during the early luteal stage (days 5–7) of the oestrous cycle. CL from early pregnancy (days 60–120) treated with BST showed a significant response in progesterone and oxytocin release. bGH showed comparable effects. Our results suggest that somatotrophin acts directly on the secretory function of bovine CL in the MDS, specifically during the early luteal stage (days 5–7) of the oestrous cycle and early pregnancy (days 60–120). Somatotrophin may therefore have physiologically relevant effects associated with the development and maintenance of luteal function. Journal of Endocrinology (1994) 143, 243–250

Effects of insulin-like growth factor-II on growth hormone release from human somatotrophinoma cells in vitro

1991 ◽  
Vol 129 (3) ◽  
pp. 447-451 ◽  
Author(s):  
P. E. Harris ◽  
M. Daniels ◽  
R. A. James ◽  
S. J. Turner ◽  
J. Dewar ◽  
...  
Keyword(s):  
Growth Factor ◽  
Hormone Release ◽  
Insulin Like Growth Factor ◽  
Inhibitory Effects ◽  
Variable Effect ◽  
Gh Secretion ◽  
Factor Ii ◽  
Igf I ◽  
Stimulation Of

ABSTRACT Insulin-like growth factor-I (IGF-I) and IGF-II receptors have previously been demonstrated on membranes prepared from human somatotrophinomas. IGF-I has been shown to have a variable effect on GH secretion by these tumours in vitro. The effects of purified IGF-II on GH secretion have not been described. We have studied the direct actions of human recombinant IGF-II on GH release from eight somatotrophinomas cultured in vitro. Somatotrophinoma cells were cultured as monolayers at a density of 105 cells/0·5 ml. Treatment with IGF-II for 4 and 24 h resulted in discrete inhibitory effects on GH release from two tumours (tumour 5:4 h, IGF-II 0·5 nmol/l; tumour 2; 24 h, IGF-II 1 nmol/l). Treatment with IGF-II for 24 h resulted in significant inhibitory effects on GH release from one tumour over a range of concentrations tested (IGF-II 0·5–10 nmol/l). Addition of human GH-releasing factor (hGRF)(1–44) (20 nmol/l) for 4 and 24 h resulted in stimulation of GH release by five tumours. Two tumours demonstrated significant inhibitory effects of IGF-II on GRF-stimulated GH release (tumour 2: 24 h, IGF-II 1–5 nmol/l; tumour 3; 4 h, IGF-II 5 nmol/l; 24 h, IGF-II 0·5–50 nmol/l). These data emphasize the heterogeneity of somatotrophinomas in terms of their response to modulators of GH secretion. IGF-II does not appear to have a modulatory role on GH release by most somatotrophinomas. Journal of Endocrinology (1991) 129, 447–451

THE SEROTONIN RETAINING EFFECT OF LITHIUM IN THE RAT THYROID

1976 ◽  
Vol 82 (2) ◽  
pp. 530-534 ◽  
Author(s):  
H. Vejlsted ◽  
O. Korsgaard
Keyword(s):  
Thyroid Hormone ◽  
Inhibitory Action ◽  
Hormone Secretion ◽  
Serotonin Release ◽  
Hormone Release ◽  
Rat Thyroid ◽  
Stimulation Of

ABSTRACT The hypothesis of a lithium induced serotonin retention in the rat thyroid has been tested. It has been found that the thyroid in rats treated with lithium contains double the amount of serotonin compared with glands from untreated animals. The ability of TSH to stimulate serotonin release is inhibited by lithium. The ability of serotonin to stimulate thyroid hormone secretion in vitro is documented. The inhibitory action of lithium on both TSH and serotonin stimulation of hormone release is documented. The serotonin retaining effect of lithium as part of the goitrogenic effect of this ion is discussed.

T3 releasing activity by Graves' sera from Graves' thyroid in vitro

1986 ◽  
Vol 111 (4) ◽  
pp. 487-493 ◽  
Author(s):  
Rudolf Hoermann ◽  
Reinhard Mueller ◽  
Bernhard Saller ◽  
Klaus Mann
Keyword(s):  
Radioreceptor Assay ◽  
Biologically Active ◽  
Graves Disease ◽  
Inhibiting Activity ◽  
Hormone Release ◽  
Serum Samples ◽  
The Individual ◽  
Camp Formation ◽  
Stimulation Of

Abstract. The insensitivity of Graves' thyroid to stimulation of cAMP formation by TSH as well as Graves' immunoglobulins in vitro is well known. The present study was performed to find out Graves' sera which may induce a final activation i.e. stimulation of T3 release in Graves' thyroid slices despite this insensitivity of tissue and to characterize determinants responsible for the efficiency of those sera. Out of 20 sera from patients with active untreated Graves' disease 6 were found to stimulate T3 release from Graves' thyroid in vitro. These 6 sera were effective in stimulating different Graves' glands, irrespective of pretreatment with propranolol, thiamazole (methimazole) or thiamazole plus iodine. In contrast, a significant response to bTSH was not observed in any Graves' gland. For comparison, 17/20 of the same sera were able to stimulate T3 release when tested on human goitrous thyroid. Sera which stimulated Graves' slices revealed no higher stimulating activities in goitrous tissue than serum samples which did not. All sera were additionally assessed for TSH binding inhibiting immunoglobulins in a radioreceptor assay. Remarkably, Graves' thyroid stimulating sera had a low or absent TSH binding inhibiting activity. Thus, hormone release from Graves' thyroid in vitro – in contrast to that from goitrous tissue – could only be activated by a minority of Graves' sera. These Graves' thyroid stimulating sera could be characterized to contain a selected spectrum of biologically active antibodies with a high TSH agonistic potency stimulating in the presence of a negligible TSH binding inhibiting activity. We conclude the qualitative composition of the antibody spectrum in the individual sera, such as the occurrence of so-called 'TSH superagonists', rather than the height of antibody titre as determined by various methods seems to be relevant for their Graves' thyroid stimulating potency.

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