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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the possible role of oxytocin in osmoregulation and its response to stress, plasma immunoreactive oxytocin was measured during hypertonic saline infusion and insulin-induced hypoglycaemia in a group of normal subjects, four patients with idiopathic diabetes insipidus and one patient with DIDMOAD syndrome (the syndrome of diabetes insipidus, diabetes mellitus, optic atrophy and deafness). The results were compared with those of plasma immunoreactive vasopressin to the same stimuli. As expected, there was a rise in plasma vasopressin in the normal subjects to both tests: this was absent in the patients with diabetes insipidus. Plasma oxytocin did not rise during hypertonic saline infusion in either group of subjects. The response of oxytocin to insulin-induced hypoglycaemia (0.15 U/kg soluble insulin) in normal subjects was much more variable. One highly symptomatic volunteer showed a marked rise in oxytocin. Two subjects also showed a rise when retested with 0.19 U/kg soluble insulin. There was no response of oxytocin to a standard-dose insulin test in the patients with diabetes insipidus. The data suggest that, in man, oxytocin is not involved in osmoregulation but that it may be secreted in response to marked hypoglycaemia.
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PMID:Responses of neurohypophysial peptides to hypertonic saline and insulin-induced hypoglycaemia in man. 351 6

Release of human neurophysin I (hNp I) and neurophysin II (hNp II) during insulin-induced hypoglycemia was studied in 10 unipolar depressed women before and after 4-5 weeks of standard antidepressant drug treatment with daily intravenous infusions of clomipramine. Before treatment, a significant increase of hNp I but not of hNp II serum levels in response to hypoglycemia was observed. At retest during clomipramine administration, a marked clinical amelioration occurred in all patients as determined with the Hamilton Rating Scale for Depression; the hNp I response to insulin was abolished, but no effect on hNp II concentration could be demonstrated. No correlation was found between the degree of the depression score decrease and the amplitude of the inhibition of hNp I release or serum levels of clomipramine or its metabolite, desmethylclomipramine. The meaning of this difference in reactivity of the neurohypophyseal system in the course of depressive illness, based on the pharmacological and biochemical profiles of clomipramine action, is discussed.
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PMID:Release of human neurophysin I during insulin-induced hypoglycemia in depressed patients is abolished after recovery with clomipramine treatment. 388 65

Oxytocin has been suggested to have behavioral effects opposite to those of vasopressin, and exogenous vasopressin is known to induce ACTH release in man. Thus, we tested the influence of exogenous oxytocin on blood levels of ACTH and cortisol during insulin-induced hypoglycemia and after vasopressin injection. Our results demonstrate an inhibitory effect of exogenous oxytocin on ACTH release and support the hypothesis of a reciprocal, balanced modulation of behavioral and neuroendocrine function by the two closely related neurohormones, vasopressin and oxytocin.
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PMID:Inhibitory influence of exogenous oxytocin on adrenocorticotropin secretion in normal human subjects. 629 May 21

In order to establish whether nitric oxide (NO) participates in the regulation of arginine-vasopressin (AVP) and/or oxytocin (OT) secretion in humans, six normal men were treated with placebo (normal saline) or the NO synthase inhibitor N,G-nitro-L-arginine methyl ester (L-NAME), given at doses (40 micrograms kg-1 injected plus 50 micrograms kg-1 infused i.v.) previously found to be unable to change blood pressure. Experiments were carried out both in basal conditions and during stimulation of posterior pituitary secretion with insulin (0.15 IU kg-1)-induced hypoglycaemia. The administration of saline or L-NAME alone was unable to change basal AVP or OT levels. Insulin-induced hypoglycaemia, however, enhanced plasma AVP and OT levels by two-fold in the absence of L-NAME and by four-fold in the presence of the NO synthase inhibitor (NOS). Blood glucose levels decreased in a similar manner during the insulin tolerance tests, regardless of L-NAME administration. In all experiments, AVP and OT responses to hypoglycaemia followed a similar pattern, with mean peak levels at 45 min. These data suggest that in normal men NO is not involved in regulation of basal AVP and OT secretions, whereas it exerts an inhibitory role in the control of the posterior pituitary hormone responses to hypoglycaemia.
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PMID:Inhibitory control of nitric oxide on the arginine-vasopressin and oxytocin response to hypoglycaemia in normal men. 753 64

The neurohypophysial peptide oxytocin (OT) is released in response to different stressors and has been suggested as a 'stress hormone'. In addition, we have recently shown that centrally administered histamine (HA), which is a mediator of stress-induced release of ACTH and prolactin (PRL), stimulates OT secretion. The aim of the present investigation was to further characterize the HA-induced OT secretion with respect to the type of postsynaptic receptor involved and to investigate the possible role of OT in HA- and stress-induced ACTH and PRL secretion. We studied (1) the effect of HA, HA agonists and HA antagonists on OT secretion in normal male rats, (2) the secretion of OT in response to HA stimulation and to restraint stress, endotoxin stress [lipopolysaccharide (LPS) administration] and insulin/hypoglycemia stress and compared the OT response to that of arginine vasopressin (AVP), (3) the OT response to restraint stress or HA in normal and AVP-deficient Brattleboro rats (DI) suffering from diabetes insipidus and (4) the effect of inhibiting the oxytocinergic system by immunoneutralization or receptor blockade on HA- and stress-induced ACTH and PRL release in normal as well as in DI rats. HA, an H1 and an H2 receptor agonist, stimulated the OT secretion dose-dependently. The HA-induced release of OT was inhibited by pretreatment with an H1 or an H2 receptor antagonist. Restraint stress and HA but not LPS or insulin stress induced an increase in peripheral OT levels, whereas only LPS stress and HA caused an increase in circulating AVP levels. Neither an OT antiserum nor an OT antagonist inhibited the HA- or restraint-stress-induced ACTH or PRL release in normal rats. AVP-deficient DI rats showed, in comparison with their nondeficit counterparts, an increased basal level of OT and no increase in OT levels following restraint stress, whereas the OT response to HA was similar in the two rat types. In AVP-deficient rats immunoneutralization of OT had no inhibitory effect on the HA- and restraint-stress-induced ACTH and PRL response. The ACTH and PRL response to restraint stress and the ACTH response to HA was impaired in DI rats compared to their healthy controls. We conclude (1) that HA stimulates OT secretion via activation of postsynaptic H1 and H2 receptors, and (2) that, in contrast to AVP, OT does not seem to be involved in HA- and restraint-stress-induced ACTH and PRL secretion.
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PMID:Involvement of oxytocin in histamine- and stress-induced ACTH and prolactin secretion. 765 94

Colchicine blockade of axonal transport from the paraventricular nucleus to the median eminence was used to indirectly infer hypothalamic ACTH secretagog release in awake rats. Median eminence contents of CRF, arginine vasopressin (AVP) and oxytocin (OT) were determined by RIA after insulin-induced hypoglycemia, restraint, and novelty. Insulin decreased circulating glucose concentrations and increased ACTH and corticosterone values. Median eminence CRF and AVP content declined but OT content did not. Both novelty and restraint stressors increased circulating ACTH and corticosterone concentrations. Secretagog measurements indicated decreases in OT content without concomitant decreases in either CRF or AVP with both stressors. These results indicate that: 1) colchicine blockade of axonal transport is useful in studying patterns of secretagog release in animals undergoing psychological stressors; 2) in contrast to physical stressors, OT appears to be a major component of the hypothalamic-pituitary-adrenal response to psychological stress; 3) the patterns of secretagog release differ with regards to physical and psychological stressors.
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PMID:Patterns of adrenocorticotropin secretagog release with hypoglycemia, novelty, and restraint after colchicine blockade of axonal transport. 767 13

Hypothalamic mechanisms of neurohormone regulation of endocrine pancreas in diabetes mellitus, adaptation to hypoxia and their combination were studied on Wistar rats. To evaluate the condition of supraoptic nucleus (SON) secretory function, paraventricular subnuclei (PVH) of hypothalamus and endocrine pancreas, we used radioimmunoassay, immunocytochemical, morphometrical and histochemical methods. Hyperglycemia, hypoinsulinemia, glucagon and somatostatin synthesis and secretion intensification in diabetes mellitus is accompanied by marked reorganization of hypothalamic neurohormones (CRF, vasopressin, oxytocin) secretion with corresponding signs of activity increase of synthesizing their hypothalamus nuclei and subnuclei and also ACTH, corticosterone, cortisol rise in blood. Adaptation to hypoxia caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF concentration, corticosterone and cortisol, ACTH in blood was not changed, vasopressin concentration lowered, oxytocin in median eminence of hypothalamus increased to a higher degree than in diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) in diabetes mellitus, hypothalamic neurohormones participating in this process.
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PMID:[The vasopressin-, oxytocin- and corticoliberin-synthesizing structures of the hypothalamus in rats with diabetes mellitus under hypoxic exposures]. 790 84

Hyperglycemia, hypoinsulinemia, and an increase of glucagon and somatostatin concentration under diabetes mellitus are accompanied by intensification of secretion of hypothalamic neurohormones (CRF, vasopressin, oxytocin, somatostatin) with the corresponding signs of the increase in activity of hypothalamus nuclei and subnuclei secreting them as well as ACTH, corticosterone and cortisol rise in blood. Adaptation to hypoxia has caused hypoglycemia, activated insulin biosynthesis, changed glucagon and somatostatin synthesis and secretion. CRF corticosterone, cortisol and ACTH concentration in blood was not changed, vasopressin concentration lowered, somatostatin and oxytocin amount (in hypothalamus) increased to a higher degree than under diabetes. Adaptation to hypoxia corrected impaired hormone balance and state of Langerhans islets (beta-cells destruction process inhibition, insulin biosynthesis stimulation, glucagon and somatostatin secretion decrease) under diabetes mellitus, hypothalamus neurohormones participating in this process.
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PMID:[Hypothalamic mechanisms of neurohormone regulation of the endocrine part of the pancreas]. 790 82

The present study was carried out in order to establish possible alterations in oxytocin (OT) secretion with aging. Therefore, we evaluated the OT responses to insulin (0.15 U/kg)-induced hypoglycemia or to the administration of angiotensin II (i.v. infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg min; each dose for 20 min) or apomorphine (60 micrograms/kg s.c.) in male subjects aged 22-80 yr and divided into 3 groups by age (group I (n = 9): 22-38 yr; group II (n = 9): 41-60 yr; group III (n = 9): 63-80 yr). Basal OT concentrations were similar in all groups. The OT response during the insulin tolerance test and the administration of ANG II had similar patterns and magnitudes in all groups. The OT response to apomorphine was similar in the two younger groups, with plasma OT levels increased 118% vs. baseline. In contrast, apomorphine was unable to induce a significant OT rise in the oldest group. During apomorphine test plasma OT concentrations were significantly lower in group III than in groups I and II. For the first time in elderly human subjects, these data show normal responsiveness of the OT secretory system to releasing stimuli such as hypoglycemia and ANG II. These findings indicate that in aged men production of OT and capability of responding to challenging stimuli is unchanged. On the other hand, the reduced OT responsiveness to apomorphine in group III might be an expression of the general dopaminergic dysfunction affecting the aging brain.
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PMID:Oxytocin response to challenging stimuli in elderly men. 805 13

Neuroendocrine response to stress stimuli is aimed to maintain body homeostasis. The activation of the neuroendocrine system is accomplished mainly by two ways: by feedback regulation based on the recognition of altered metabolic homeostasis by appropriate receptors sending the signal into the CNS, and by forward regulation involving a direct stimulation of the neuroendocrine system by a central command coming from an activated brain regulatory center. With regard to mechanisms of neuroendocrine activation, the signal specificity and site of its origin are of particular importance. The significance of the signal in neuroendocrine responses has been evaluated in three different stress conditions: hypoglycemia, surgical trauma and dynamic physical exercise. The stimulus inducing neuroendocrine response during hypoglycemia is the glucopenia. The signal for the activation of the neuroendocrine response is generated in glucosensitive cells which are not located in a single brain structure (hypothetical glucostat). The signal for growth hormone, vasopressin and oxytocin release is produced in brain structures protected by the blood-brain barrier, that for ACTH release in regions both protected and unprotected by the barrier, while the signal for prolactin release is generated in tissues lacking the blood-brain barrier. The neuroendocrine response during surgical trauma is activated by a signal formed in the damaged tissue reaching the CNS by neural pathways. Moreover, cytokins may participate on endocrine stimulation in those surgical interventions in which a large amount of bacterial endotoxins is released. During a complicated surgery, e.g. during a bypass other signals and modifying factors, such as hypothermia, dilution of blood, hypoperfusion of organs, rewarming of the body and hormone degradation in the oxygenator are important. On the On the other hand, during a short-term dynamic exercise, a forward regulation by a central signal from the activated CNS motor center comes into play with the consequent release of catecholamines, growth hormone, etc. In the control of some other hormones (beta-endorphin, partly ACTH) and especially during a long term exercise, neural signals from working muscles (feedback) are also involved. During a static exercise mainly catecholamines triggered by signals from working muscle cells are activated. The understanding of the signal and mechanisms of neuroendocrine activation during stress is indispensable for selective modulation of physiological and pathological responses.
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PMID:[Activation of the neuroendocrine system during changes in homeostasis during stress conditions]. 868 9


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