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

The hypothesis that electrotonic spread among oxytocinergic neurons contributes to synchronized bursting in the lactating rat leads to the prediction that coupling among oxytocinergic neurons would be stronger and more abundant in lactating than in non-lactating animals. We tested this prediction using, as an index of electrical coupling, transfer among neurons of the fluorescent dye Lucifer Yellow CH, which crosses gap junctions. Intracellular injections (total of 159) of the dye were made in supraoptic nucleus neurons in hypothalamic slices from virgin female and lactating rats. In virgins, 86 injections resulted in 76 single, 8 coupled pairs and 2 triplets of dye-filled neurons. In contrast, 73 injections in lactators yielded 51 single, 16 coupled pairs and 6 triplets, (greater than 100% increase) a difference significant at P less than 0.001. Immunocytochemical identification of the dye-filled cells revealed that there was an increase over virgins in coupling among both oxytocinergic and vasopressinergic neurons. These results are consistent with the hypothesis that electrical coupling is involved in synchronizing oxytocin cell bursting in lactators. They are also consistent with published data indicating that vasopressin neurons are metabolically activated (show increased glucose uptake) during suckling and may show correlated activity.
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PMID:Dye coupling among immunocytochemically identified neurons in the supraoptic nucleus: increased incidence in lactating rats. 281 70

The effects of hormones on phosphoinositide metabolism were examined in rat adipocytes prelabeled with 32Pi or [3H]inositol. Oxytocin and vasopressin produced large decreases in labeled polyphosphoinositides and increases in phosphatidic acid and inositol phosphates, whereas insulin was without effect, although it stimulated lipogenesis from glucose. Likewise, insulin did not elevate 1,2-diacylglycerol measured chemically by high pressure liquid or thin-layer chromatography in fat cells or pads. It also did not increase the radioactivity in 1,2-diacylglycerol in ghosts prepared from fat cells previously labeled with [3H]arachidonic acid, although oxytocin and vasopressin increased this. It is therefore concluded that insulin does not stimulate the breakdown of polyphosphoinositides to yield 1,2-diacylglycerol and inositol phosphates in adipocytes and that the insulin-like actions of oxytocin must be due to other changes. Insulin induced small, but significant and equal increases (40% at 30 min) in the incorporation of [3H] inositol into phosphatidylinositol, phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate in adipocytes. The effects were not dependent upon glucose and were not evident before 15 min. Oxytocin also produced large increases in the labeling of the three phosphoinositides. Insulin stimulated the incorporation of [3H]glycerol into the three phosphoinositides and also phosphatidic acid, phosphatidylserine, and phosphatidylethanolamine by 50-100% in cells incubated without glucose. No changes in the labeling of glycerol 3-phosphate, lysophosphatidic acid, phosphatidylcholine, and triacylglycerol were detected, and there was a small increase (30%) in 1,2-diacylglycerol labeling. It is concluded that insulin increases the synthesis of phosphatidylinositol, phosphatidylinositol 4-phosphate, phosphatidylinositol 4,5-bisphosphate, phosphatidylethanolamine, and phosphatidylserine in fat cells partly by stimulating a reaction(s) located between glycerol 3-phosphate and phosphatidic acid in the biosynthetic pathway.
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PMID:Insulin and oxytocin effects on phosphoinositide metabolism in adipocytes. 283 Nov 95

To find out whether plasma vasopressin (PAVP) response to a water load during pregnancy is inappropriately high, as had been speculated, we measured PAVP by radioimmunoassay in 30 women at the time of delivery. Ten women had received infusion of aqueous glucose solution during labor for hydration (GW group); another ten received infusion of glucose solution as a vehicle for oxytocin (OT group), and ten women did not receive any intrapartum intravenous fluid therapy (controls). Serum sodium and osmolality were also determined in all the subjects. PAVP levels were significantly lower in GW (0.70 +/- 0.4 pg/ml) and OT groups (0.7 +/- 0.6 pg/ml) (P less than 0.05). Significant negative correlation was seen between the amount of glucose solution infused and levels of PAVP (r = -0.66; P less than 0.01), while a significant positive correlation was seen between PAVP and serum sodium (r = 0.61; P less than 0.01). These findings suggest that during labor, the physiological relationship between serum osmolality and PAVP is intact, and that infusion of a water load in the form of aqueous glucose solution is attended by an expected lowering of PAVP. We infer that inappropriate ADH response is not the cause of water retention and hyponatremia often seen in women receiving aqueous glucose solution during labor.
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PMID:Plasma arginine vasopressin response to water load during labor. 286 30

Injections and infusions of oxytocin into conscious dogs caused an increase in plasma concentrations of glucose, insulin and glucagon. When blood glucose was clamped at a raised level the injection of oxytocin still increased insulin and glucagon concentrations in plasma. Infusion of somatostatin suppressed plasma concentrations of glucagon and insulin but did not prevent oxytocin-induced increments in blood glucose. Injection of oxytocin still caused a marked release of glucagon, whereas the insulin response was greatly diminished. When endogenous insulin and glucagon secretion was suppressed by infusion of somatostatin and glucose levels were stabilized by concomitant infusions of glucagon and insulin, injections of oxytocin did not alter blood glucose concentrations. It is concluded that the increase in blood glucose following the administration of oxytocin is secondary to the release of glucagon and that oxytocin exerts a direct stimulatory effect on glucagon and possibly insulin secretion.
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PMID:The mechanism of the effect of oxytocin on plasma concentrations of glucose, insulin and glucagon in conscious dogs. 286 96

The plasma concentrations of the gastrointestinal regulatory peptides vasoactive intestinal polypeptide (VIP), insulin, secretin, somatostatin, motilin, pancreatic polypeptide (PP) and gastric inhibitory polypeptide (GIP), as well as blood glucose, were measured in eight healthy women before, during and after oxytocin infusion in post-term pregnancies. Plasma VIP increased significantly (P less than 0.01) during oxytocin infusion. Plasma secretin showed a significant (P less than 0.05) decrease during oxytocin infusion. Plasma somatostatin remained unchanged during oxytocin infusion, but thereafter a significant (P less than 0.05) increase occurred. Both plasma motilin and plasma PP showed a non-significant increase during oxytocin infusion with sustained levels thereafter. No changes were found for plasma insulin, GIP and blood glucose.
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PMID:Gastrointestinal regulatory peptides during oxytocin infusion in post-term pregnancies. 290 9

The changes in blood glucose, plasma oxytocin, plasma vasopressin, plasma atrial natriuretic peptide, serum osmolality, haematocrit and blood pressure were measured in response to acute insulin-induced hypoglycaemia in six normal male subjects. After the i.v. administration of insulin (0.15 U/kg), plasma concentrations of oxytocin and vasopressin increased rapidly in all subjects and were maximal 15 min after the acute hypoglycaemic reaction (R). Haematocrit increased at the time of the hypoglycaemic reaction, but there was no change in serum osmolality. Systolic blood pressure rose and diastolic blood pressure fell, but mean arterial blood pressure remained unchanged. No changes were demonstrated in plasma concentrations of atrial natriuretic peptide. The release of oxytocin and vasopressin in response to acute hypoglycaemia in man is probably caused by stimulation of the posterior pituitary gland via hypothalamic activation, and not by stimulation of osmoreceptors or baroreceptors.
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PMID:Plasma oxytocin, arginine vasopressin and atrial natriuretic peptide responses to insulin-induced hypoglycaemia in man. 295 4

The hypophysiotropic coding of ACTH secretion resulting from insulin-induced hypoglycemia was investigated in urethane-anesthetized fasted rats. The participation of corticotropin-releasing factor (CRF), arginine vasopressin (AVP), and catecholamines in the ACTH response was first investigated by systemic administration of CRF antiserum, an AVP pressor antagonist, or a ganglionic blocking agent. These treatments were without effect on the hypoglycemic response, which was characterized by a 67% fall in systemic glucose levels within 30 min of insulin administration. ACTH secretion in response to insulin-induced hypoglycemia was differentially affected by these pharmacological treatments. Administration of antiserum to CRF abolished the ACTH response, whereas ganglionic blockade was without significant effect. However, administration of a vasopressinergic pressor antagonist significantly attenuated ACTH secretion after insulin treatment. These observations suggested the participation of both CRF and AVP in mediation of the ACTH secretory response to hypoglycemia. Infusion of glucose to counter the hypoglycemia action of insulin injection prevented the ACTH secretory response. Measurement of immunoreactive (ir) CRF, irAVP, and ir-oxytocin in sequential collections of hypophysial portal plasma revealed a significant elevation of irAVP concentration without concomitant elevation of irCRF or ir-oxytocin levels. We propose that CRF functions in a permissive role, maintaining a relatively constant portal concentration and thereby allowing expression of the weaker ACTH-releasing activity of AVP and other secretagogues. Thus, AVP, not CRF, appears to represent the dynamic mediator of ACTH secretion accompanying insulin-induced hypoglycemia. These observations provide additional support for the hypothesis of multifactor stimulus-specific hypophysiotropic coding of ACTH secretion.
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PMID:Hypophysiotropic regulation of adrenocorticotropin secretion in response to insulin-induced hypoglycemia. 298 21

Effects of vasopressin (AVP), oxytocin (OXY), norepinephrine (NE), and glucose on the single-unit activity of hypothalamic ventromedial nucleus (VMN) in tissue slices were studied. While AVP was exclusively excitatory on 58% of the neurons, OXY could be excitatory or inhibitory and affected only 42% of the neurons. There was no correlation between the responses to these two peptides. Each of these two peptides could desensitize neuronal response to itself, but did not cross-desensitize responses to each other. These results indicate that AVP and OXY do not act on the same population of VMN neurons through the same cellular mechanism. Furthermore, only the responses to AVP were correlated to responses to glucose and NE, two agents relevant to central regulation of feeding. This correlation with responses to feeding-relevant agents and the exclusively excitatory action on the VMN, which is involved in the regulation of feeding, suggest that AVP can play a role in the regulation of feeding, particularly the feeding induced by the injection of NE into the paraventricular nucleus, that is known to alter AVP release.
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PMID:Vasopressin excites ventromedial hypothalamic glucose-responsive neurons in vitro. 301 71

Vasopressin and oxytocin administered subcutaneously and intravenously in a dose of 0.5 IU/kg were studied in experiments on albino male rats for their effect on the glycogen content and gluconeogenesis enzymes activity in the liver as well as on the glycemia level. Neurohormones injected subcutaneously have no effect on the values of the measured indices. Vasopressin already the first 15-60 min after its intravenous injection in the mentioned dose leads to an essential decrease of the glucose content in blood, glycogen amount, glucose-6-phosphatase and fructose-1.6-diphosphatase (EC 3.1.3.9 and 3.1.3.11) activity in the liver of test animals. The intravenous injection of oxytocin in the same dose induces changes in the carbohydrate metabolism indices similar in their direction and magnitude to the effects of intravenous injection of vasopressin.
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PMID:[The role of vasopressin and oxytocin in the regulation of glycemia levels and carbohydrate metabolism in the liver]. 303 60

Pharmacological doses of oxytocin administered in basal conditions evoked a rapid surge in plasma glucose and glucagon levels followed by a later increase in plasma insulin and adrenaline levels. The effects of oxytocin on plasma glucagon and adrenaline levels were potentiated by hypoglycemia. When the endogenous pancreas secretion was suppressed by cyclic somatostatin (150 micrograms/h) and exogenous glucagon (3.5 micrograms/h) and insulin (0.2 mU/kg.min) were both replaced, oxytocin (0.2 U/min) evoked a transient but significant increase in plasma glucose levels suppressing the glucose infusion rate (GIR) in the first 60 min. On the contrary at higher insulin infusion rate (0.6 mU/kg.min) plasma glucose levels and GIR remained unaffected throughout the study. Oxytocin seems also to potentiate glucose-induced insulin secretion as evidenced by hyperglycemic glucose clamp. In conclusion, pharmacological doses of oxytocin seem to exert a prevalent hyperglycemic effect by a combined action at the liver site (as glycogenolytic agent) and at the endocrine pancreas (as a stimulatory agent of A cell secretion).
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PMID:Pharmacological doses of oxytocin affect plasma hormone levels modulating glucose homeostasis in normal man. 306 8


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