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

The responses of serum oxytocin (OT) and vasopressin (AVP) to the serotonergic HT1A agonist buspirone (15 mg p.o.) or the HTD1 agonist sumatriptan (6 mg injected subcutaneously) were evaluated in 7 normal men either in basal conditions or during an insulin (0.15 iu/kg as an i.v. bolus) tolerance test (ITT). Neither buspirone nor sumatriptan administration modified the basal secretion of AVP and OT. Stimulation of 5HT-1D receptors with sumatriptan was unable to change neither AVP nor OT response to insulin-induced hypoglycemia. On the other hand, the pretreatment with the 5HT1A agonist buspirone significantly enhanced the OT response during hypoglycemia, without modifying the AVP rise. The results of this study suggest that serotonergic 5HT1A receptors may interact with hypoglycemia in the stimulation of OT, but not AVP secretion.
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PMID:Different effects of the serotonergic agonists buspirone and sumatriptan on the posterior pituitary hormonal responses to hypoglycemia in humans. 877 61

Previous studies have demonstrated that the nitric oxide (NO) synthase inhibitor L-NAME exerts positive effects on the arginine vasopressin (AVP) and oxytocin (OT) responses to insulin-induced hypoglycemia, suggesting inhibitory actions of NO. The present study was designed to determine whether a gamma-aminobutyric acid (GABA)ergic pathway is involved in regulation of NO action. AVP and OT secretory patterns during insulin (0.15 IU/kg, i.v.)-tolerance tests (ITT) were examined in seven normal male subjects with (experimental tests) and without (control test) concomitant treatment with L-NAME (40 micrograms/kg injected plus 50 micrograms/kg infused, i.v.), the GABAergic agent sodium valproate (600 mg in three divided doses orally) or the combination of L-NAME and sodium valproate. Insulin-induced hypoglycemia increased by 2-fold (peak vs. baseline) plasma AVP and OT levels. In the presence of L-NAME, plasma AVP and OT levels rose 3-fold in response to hypoglycemia and were significantly higher than those in the control test. Administration of sodium valproate alone changed neither AVP nor OT secretory patterns during ITT. In contrast, sodium valproate abolished the facilitating effect of L-NAME on both AVP and OT responses to hypoglycemia. In the ITT plus L-NAME plus sodium valproate test, plasma AVP and OT levels were not significantly different at any time point from those observed during the control ITT. These data indicate a GABAergic mediation of the inhibitory modulation by NO of the AVP and OT responses to insulin-induced hypoglycemia.
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PMID:Gamma-aminobutyric acid mediation of the inhibitory effect of nitric oxide on the arginine vasopressin and oxytocin responses to insulin-induced hypoglycemia. 895 1

The authors review various aspects of gestational diabetes, including definition, screening, diagnostic procedures, complications (hypertension, macrosomia), clinical evaluation (ultrasound, non-stress test), treatment (diet, insulin), indications for delivery and neonatal aspects (hypoglycaemia, hypocalcaemia). Complications can be reduced by intensive dietary treatment and insulin. If the gestational diabetes is regulated well the woman can wait for spontaneous birth at term. In the case of pregnant women with less than optimal regulated diabetes, however, or with complications such as hypertension, macrosomia, previous stillbirth, labour can be induced preterm by local administration of prostaglandin or infusion of oxytocin. Physical training and weight reduction should be instituted to avoid later development of type II diabetes mellitus. There is still some uncertainty about different aspects of gestational diabetes.
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PMID:[Pregnancy in diabetes]. 926 87

Within the central nervous system, glucagon-like peptide-1-(7-36) amide (GLP-1) acts as a transmitter, inhibiting feeding and drinking behavior. Hypothalamic neuroendocrine neurons are centrally involved in the regulatory mechanisms controlling these behaviors, and high densities of GLP-1 binding sites are present in the rat hypothalamus. In the present study we have, over a period of 4 h, followed the effect of centrally injected GLP-1 on plasma levels of the neurohypophysial hormones vasopressin and oxytocin. Plasma levels of corticosterone and glucose were also followed across time after central administration of GLP-1. In conscious, freely moving, and unstressed rats, central injection of GLP-1 significantly elevated plasma levels of vasopressin 15 and 30 min after administration (basal, 0.8 +/- 0.2 pg/ml; 15 min, 7.5 +/- 2.0 pg/ml; 30 min, 5.6 +/- 1.1 pg/ml; mean +/- SEM) and elevated corticosterone 15 min after administration (52 +/- 13 vs. 447 +/- 108 ng/ml, basal vs. 15 min; mean +/- SEM). In contrast, plasma oxytocin levels were unaffected by intracerebroventricular (icv) injections of GLP-1 over a period of 4 h after the injection. The animals given a central injection of GLP-1 developed transient hypoglycemia 20 min after the injection, which was fully restored to normal levels at 30 min. Furthermore, we used c-fos immunocytochemistry as an index of stimulated neuronal activity. The distribution and quantity of GLP-1-induced c-fos immunoreactivity were evaluated in a number of hypothalamic neuroendocrine areas, including the magnocellular neurons of the paraventricular (PVN) and supraoptic (SON) nuclei and the parvicellular neurons of the medial parvicellular subregion of the PVN. The number of c-fos-expressing nuclei in those areas was assessed 30, 60, and 90 min after icv administration of GLP-1. Intracerebroventricular injection of GLP-1 induced c-fos expression in the medial parvicellular subregion of the PVN as well as in magnocellular neurons of the PVN and SON. A slight induction of c-fos expression was seen in the arcuate nucleus and the nucleus of the solitary tract, including the area postrema. In contrast, the subfornical organ, which is a rostrally situated circumventricular organ, was free of c-fos-positive cells after central administration of GLP-1. When the GLP-1 antagonist exendin-(9-39) was given before the GLP-1, c-fos expression in these neuroendocrine areas was almost completely abolished, suggesting that the effect of GLP-1 on c-fos expression is mediated via specific receptors. A dual labeling immunocytochemical technique was used to identify the phenotypes of some of the neurons containing c-fos-immunoreactive nuclei. Approximately 80% of the CRH-positive neurons in the hypophysiotropic medial parvicellular part of the PVN coexpressed c-fos 90 min after icv GLP-1 administration. In contrast, very few (approximately 10%) of the vasopressinergic magnocellular neurons of the PVN/SON contained c-fos-positive nuclei, whereas approximately 38% of the magnocellular oxytocinergic neurons expressed c-fos-positive nuclei in response to GLP-1 administration. This study demonstrates that central administration of the anorectic neuropeptide GLP-1 activates the central CRH-containing neurons of the hypothalamo-pituitary-adrenocortical axis as well as oxytocinergic neurons of the hypothalamo-neurohypophysial tract. Therefore, we conclude that GLP-1 activates the hypothalamo-pituitary-adrenocortical axis primarily through stimulation of CRH neurons, and this activation may also be responsible for the inhibition of feeding behavior.
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PMID:Central administration of glucagon-like peptide-1 activates hypothalamic neuroendocrine neurons in the rat. 932 62

The present study was undertaken in order to establish the possible involvement of 5-HT3 serotonergic receptors in the control of basal and/or hypoglycemia-stimulated arginine vasopressin (AVP) and/or oxytocin (OT) secretion. For this purpose, 12 normal men were injected intravenously with a bolus of 4 mg ondansetron, a specific 5-HT3 receptor antagonist, under basal conditions (n = 6) or 30 min before insulin (0.15 IU/kg body weight) administration (n = 6) (insulin tolerance test (ITT)). Control experiments with normal saline instead of ondansetron treatment were performed. Furthermore, on a different occasion, the same subjects were tested in identical experimental conditions with 8 mg ondansetron. Our results showed that the hypoglycemic response to insulin was similar during the ITT and ondansetron plus ITT. Inhibition of 5-HT3 serotonergic receptors with ondansetron (4 or 8 mg) did not modify the basal secretion of AVP and OT and the OT response to insulin-induced hypoglycemia. In contrast, the administration of 4 or 8 mg ondansetron significantly reduced in a similar manner hypoglycemia-induced AVP rise. Mean peak level at 45 min after insulin injection was 2.25 times higher than baseline in the control ITT and 1.5 times higher than basal value in the ondansetron (4 or 8 mg) plus ITT. These data demonstrate that 5-HT3 serotonergic receptors at least partially mediate the AVP response to hypoglycemia, without modifying the simultaneous OT response. On the other hand, 5-HT3 receptors do not appear to be involved in the control of basal posterior pituitary hormone secretions.
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PMID:5-HT3 serotonergic receptor mediation of hypoglycemia-induced arginine-vasopressin but not oxytocin secretion in normal men. 963 16

In order to establish whether melatonin alters basal and/or stimulated oxytocin secretion, 18 normal men were treated (p.o.) with 6 or 12 mg melatonin or placebo in basal conditions (N-6 subjects) or concomitantly to the administration of insulin (O.15 IU/kg body weight in an i.v. bolus) (N-6 subjects) or angiotensin II (increasing doses of 4, 8 and 16 ng/kg/min, at intervals of 20 min). The administration of 6 or 12 mg melatonin did not change basal and angiotensin II-stimulated oxytocin secretion. In contrast, the oxytocin response to insulin-induced hypoglycemia was significantly reduced by melatonin treatment. In fact, the mean peak oxytocin response to hypoglycemia was 2.2 times higher than baseline in the absence of melatonin, whereas it was 1.6 times higher than basal value after administration of 6 or 12 mg melatonin. These data indicate an involvement of melatonin in the regulation of the oxytocin response to hypoglycemia in normal men. The lack of effects of melatonin on basal and angiotensin II-stimulated oxytocin secretion argues against the possibility that melatonin exerts an overall modulatory role on oxytocin secretion in humans.
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PMID:Melatonin inhibits oxytocin response to insulin-induced hypoglycemia, but not to angiotensin II in normal men. 966 95

The neurohypophysial hormones oxytocin and vasopressin show daily rhythms of secretion with elevated hormone release during the hours of sleep. This pattern can be modulated by ovarian steroids and alters with age. The pattern appears to be due in part to the nocturnal increase in melatonin secretion, which stimulates hormone release in man, while being inhibitory in the rat. Pinealectomy alters both the 24 h pattern of neurohypophysial hormone release in the rat and the firing rate of magnocellular supraoptic nucleus neurones. There is also a reduced hormone release in response to hypovolaemia and raised plasma sodium concentration compared to sham operated animals, with a smaller increase in neuronal activity, as determined by immediate-early gene expression. The normal responses can be restored by nocturnal administration of melatonin. Melatonin also influences the neurohypophysial hormone response in the human to known stimuli of release, such as raised plasma osmolality, exercise and insulin-induced hypoglycaemia. Recent studies have revealed that not only does the release of vasopressin and oxytocin vary over each 24 h, but the respective renal and pregnant uterine responses also show diurnal variations.
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PMID:Diurnal rhythms in neurohypophysial function. 1079 21

Obstetrical and perinatal outcomes in newborns of diabetic pregnant women depend on metabolic control and fetal surveillance during pregnancy. The effects of fetal surveillance on perinatal mortality and morbidity was analyzed in diabetic pregnant women with appropriate glucose control in our regional center for diabetes and pregnancy. 480 deliveries complicated by frank or gestational diabetes occurred in our Department in the period of 1988-1999. Perinatal mortality and morbidity, prevalence of premature deliveries, methods of fetal surveillance, options for respiratory distress syndrome (RDS) profilaxis, cesarean section rate, timing of delivery and its indications and occurrence of malformations have been analyzed. It was found that malformation rate and perinatal mortality may be reduced to even lower level than that of in healthy pregnant women by appropriate glucose control and by using the latest methods of intrauterine fetal surveillance including cardiotocography (non stress test and oxytocin challenge test), doppler fetal artery velocimetry and fetal pulse oximetry. Timing of delivery was needed in 35% of the cases with IDDM and 15% of gestational diabetes due to chronic placental insufficiency. If labour induction was needed before the 38 weeks, amniocentesis was performed to test fetal lung maturity. Direct fetal glucocorticoid administration was used to enhance fetal lung maturation in 14 cases. C-section rate was slightly higher than that of in non diabetic pregnant women. Our perinatal morbidity data (macrosomia, hyperbilirubinemia, hypoglycemia, injuries, infections) are comparable with the data from the literature. Although perinatal mortality with the help of thorough fetal surveillance is even better in diabetic pregnant women than in non diabetic patients, future eye should be focused on factors affecting perinatal morbidity, because it is still higher than in newborns of healthy mothers.
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PMID:Improvement of perinatal outcome in diabetic pregnant women. 1175 14

Orexin (hypocretin)-containing projections from lateral hypothalamus (LH) are thought to play an important role in the regulation of feeding behaviour and energy balance. In rodent studies, central administration of orexin peptides increases food intake, and orexin neurones in the LH are activated by hypoglycaemia during fasting. In addition, administration of orexins into the fourth ventricle or the dorsal motor nucleus of the vagus (DMV) has been shown to stimulate gastric acid secretion and motility, respectively, via vagal efferent pathways. In this study, whole-cell recordings were obtained from DMV neurones in rat brainstem slices to investigate the cellular mechanism(s) by which orexins produce their gastrostimulatory effects. To determine whether responsiveness to orexins might be differentially expressed among distinct populations of preganglionic vagal motor neurones, recordings were made from neurones whose projections to the gastrointestinal tract had been identified by retrograde labelling following apposition of the fluorescent tracer DiI to the gastric fundus, corpus or antrum/pylorus, the duodenum or caecum. Additionally, the responses of neurones to orexins were compared with those produced by oxytocin, which acts within the DMV to stimulate gastric acid secretion, but inhibits gastric motor function. Bath application of orexin-A or orexin-B (30-300 nM) produced a slow depolarization, accompanied by increased firing in 47 of 102 DMV neurones tested, including 70 % (30/43) of those that projected to the gastric fundus or corpus. In contrast, few DMV neurones that supplied the antrum/pylorus (3/13), duodenum (4/18) or caecum (1/13) were responsive to these peptides. The depolarizing responses were concentration dependent and persisted during synaptic isolation of neurones with TTX or Cd2+, indicating they resulted from activation of postsynaptic orexin receptors. They were also associated with a small increase in membrane resistance, and in voltage-clamp recordings orexin-A induced an inward current that reversed near the estimated equilibrium potential for K+, indicating the depolarization was due in large part to a reduction in K+ conductance. Orexins did not affect synaptically evoked excitation, but did reduce membrane excitability in a subset of gastric-projecting DMV neurones by enhancing GABA-mediated synaptic input. Lastly, although many DMV neurones responded to orexins and oxytocin with excitation, for the most part these peptides modulated excitability of distinct populations of gastric-projecting vagal motor neurones. These results indicate that orexins act preferentially within the DMV to directly excite vagal motor neurones that project to gastric fundus and corpus. In this way, release of endogenous orexins from descending hypothalamic projections into the DMV may mediate the increase in gastric acid secretion and motor activity associated with the cephalic phase of feeding.
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PMID:Gastrointestinal-projecting neurones in the dorsal motor nucleus of the vagus exhibit direct and viscerotopically organized sensitivity to orexin. 1267 67

The objective was to evaluate the influence of patient-controlled epidural analgesia (PCEA) using low doses of bupivacaine vs. ropivacaine, on labor pain, motor blockade, progression of labor, delivery and neonatal outcome. This randomized double blind study included 565 parturients. All received a 5-mL/h infusion and PCEA (5-mL boluses with a 20-min lockout, maximum volume 20 mL/h) of either 0.125% bupivacaine (n = 313: 165 nulliparous, 148 parous) or 0.2% ropivacaine (n = 252: 113 nulliparous, 139 parous). Pain score, lower limb motor block, sensory levels, local analgesic doses required, hemodynamic parameters, side effects and complications were assessed. Obstetric variables included cervical dilation at epidural insertion, incidence of ruptured membranes and their duration, use of oxytocin, fetal heart rate changes, duration of labor, mode and outcome of delivery, and use of invasive and non-invasive fetal monitoring. Neonatal characteristics included birth weight, Apgar scores, umbilical artery pH, serum bilirubin, hypoglycemia, need for assisted ventilation, sepsis or sepsis study, feeding difficulties and respiratory distress syndrome. Ropivacaine 0.2% was equianalgesic with 0.125% bupivacaine, but produced less motor block (P < 0.0001). There were no significant differences, however, in duration of labor, delivery type or neonatal outcome.
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PMID:Patient-controlled epidural analgesia for labor pain: effect on labor, delivery and neonatal outcome of 0.125% bupivacaine vs 0.2% ropivacaine. 1532 32


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