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

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

Colocalization of thyrotropin-releasing hormone-like immunoreactivity with other neuroactive substances was examined immunohistochemically in colchicine-treated rat brains using double-staining or elution-restaining methods. Thyrotropin-releasing hormone-like immunoreactivity was shown to be located in the same neurons as: 1. enkephalin-, gamma-amino butyric acid- and tyrosine hydroxylase-, but not somatostatin-like immunoreactivity in the glomerular layer of the olfactory bulb 2. oxytocin- and cholecystokinin-, but not vasopressin-like immunoreactivity in the supraoptic nucleus 3. cholecystokinin-like immunoreactivity in posterior pituitary 4. enkephalin-like immunoreactivity in the perifornical area of the hypothalamus and 5. neuropeptide Y- and neurotensin-like immunoreactivity in the periaqueductal central grey. These findings provide further examples of coexistence of thyrotropin-releasing hormone with classical neurotransmitters and/or peptides in the rat central nervous system.
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PMID:Coexistence of TRH with other neuroactive substances in the rat central nervous system. 315 46

Intrathecal (IT) injection of arginine vasopressin (AVP) in rats caused a transient (less than 30 min), dose-related paralysis of the hindlimbs, loss of hindlimb and tail nociceptive responsiveness, and increased mean arterial pressure. Motor dysfunction was produced with comparable potency by lysine vasopressin (LVP) and arginine vasotocin (AVT); oxytocin (OXY) was approximately 1000 times less potent. Paralysis induced by these peptides was selectively blocked following IT pretreatment with 0.5 nmoles of the vasopressin V1 receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(O-methyl)tyrosine] Arg8-vasopressin (d(CH2)5[Tyr(Me2)]AVP). Pressor and antinociceptive responses to AVP were also blocked by this compound. However, at higher doses (2-5 nmoles, IT), d(CH2)5[Tyr(Me2)]AVP produced hindlimb paralysis, antinociception, and pressor responses by itself. In contrast to the fiber degeneration, cell loss, and necrosis found in lumbosacral cords of rats persistently paralyzed by other peptides (dynorphin A, somatostatin, and ICI 174864), neuropathological changes were not evident in spinal cords of rats transiently paralyzed by IT AVP. These results indicate that AVP-related peptides affected diverse spinal cord functions through interactions with a V1-like receptor. The similar pattern of cardiovascular and antinociceptive responses to other peptides (dynorphin A, somatostatin, and ICI 174864), which also caused hindlimb paralysis, suggests that the former responses may actually reflect the nonselective consequences of a peptide-induced disruption of spinal cord function, rather than specific shared pharmacological effects.
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PMID:Hindlimb paralytic effects of arginine vasopressin and related peptides following spinal subarachnoid injection in the rat. 324 52

Recent reports indicate that oxytocin exerts direct effects on the release of insulin and glucagon from the endocrine pancreas of the rat. The purpose of this study was to determine whether oxytocin-like immunoreactivity is present in the anglerfish islet, and if it is associated with subsets of hormone-producing cells. Antisera against oxytocin, insulin, glucagon, somatostatin, neuropeptide Y, and the 200-kd neurofilament polypeptide were applied to serial 5 micrometers sections of pancreatic islets. The antiserum to the 200-kd neurofilament polypeptide labeled nerve bundles and axons, some of which were also stained with the oxytocin antiserum. Oxytocin immunoreactivity was observed in large nerves that branched into varicose fibers. These fibers were consistently associated only with clusters of insulin-producing cells. Successive application of oxytocin and insulin antisera to the same section provided additional verification of this relationship. Oxytocin-labeled nerves were not associated with cells immunoreactive to glucagon, somatostatin, or neuropeptide Y (anglerfish peptide Yg). The results demonstrate that oxytocin or an oxytocin-like peptide is located in fibers that surround only insulin-producing cells in the anglerfish islet. Although the functional significance of this observation remains to be determined, the results imply that oxytocin, or an oxytocin-like peptide, may affect the synthesis or release of insulin from anglerfish islets.
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PMID:Oxytocin-like immunoreactive nerves are associated with insulin-containing cells in pancreatic islets of anglerfish (Lophius americanus). 330 46

This paper presents data showing that the sympathetic autonomic areas of the cat thoracolumbar spinal cord contain nerve terminals and fibres with immunoreactivity for at least seven neuropeptides. The distribution in the intermediolateral cell column of the terminals and fibres which contain enkephalin-, neuropeptide Y-, neurotensin-, substance P-, and neurophysin II-like immunoreactivity (ENK, NPY, NT, SP, and NP2, respectively) suggests that these peptides are involved in more generalized functions of the autonomic nervous system. On the other hand, peaks in density of immunoreactivity at certain levels suggest that different levels of influence of sympathetic preganglionic neurons by the various peptides may occur along the length of the thoracolumbar cord. The distribution of terminals and fibres containing somatostatin- and oxytocin-like immunoreactivity (SS and OXY) suggests that these peptides may be part of specific pathways to particular sympathetic preganglionic neurons. The possible sources of the terminals and fibres containing ENK, NPY, NT, SS, and SP include the spinal cord and supraspinal areas, whereas the source of these structures with OXY and NP2 is most likely supraspinal. The data suggest that coexistence of peptides and interactions between structures containing different neuropeptides occur in the spinal autonomic areas. It is speculated that neuropeptides have an important role to play in the regulation of the cardiovascular division of the autonomic nervous system.
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PMID:Peptidergic inputs to sympathetic preganglionic neurons. 331 10

The dose and time treatment effects of arginine vasopressin (AVP) on basal and hCG-stimulated testosterone accumulation by purified mouse Leydig cells in primary culture were examined. Pretreatment for 24 h of Leydig cells with AVP caused a stimulation of the acute (3 h) basal testosterone accumulation. In these conditions, progesterone accumulation was also increased. The stimulatory effect of AVP (10(-11)-10(-5) M) on testosterone accumulation was dose-dependent and as little as 10(-11) M-AVP caused significant stimulation whilst maximal effect was achieved with 10(-7) M. Oxytocin (10(-6) M) also showed a stimulation of testosterone accumulation in basal conditions, but the other peptides tested at the same concentration (neurotensin, somatostatin and substance P) did not have any effect. When Leydig cells were exposed to AVP for a longer period (48 or 72 h), the increase in basal testosterone accumulation disappeared. AVP treatment of Leydig cells for 72 h led to a significant and dose-dependent reduction in the hCG-responsiveness without altering the slope of the hCG dose-response curve. This inhibitory effect, which was also observed when AVP-pretreated Leydig cells were acutely challenged for 3 h with 8-bromo-cAMP, was accompanied by a concomitant increase in progesterone accumulation. These results indicate that AVP can exert a dual effect on mouse Leydig cells: stimulatory on basal testosterone accumulation during short-term exposure (24 h) and inhibitory on the response to hCG stimulation after long-term treatment (72 h). They provide additional evidence that neurohypophysial peptides directly affect Leydig cell steroidogenesis.
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PMID:Time-related effects of arginine vasopressin on steroidogenesis in cultured mouse Leydig cells. 333 82

The hypothalamic systems secreting corticotropin-releasing hormone (CRF), somatostatin, oxytocin, vasopressin and luteinizing hormone-releasing hormone (LHRH) were characterized using immunochemistry, and variations were studied in relation to the recrudescence of testicular activity in the ferret and the mink, two species with opposite photoregulation of their annual reproductive cycles. Under the present conditions of study, the immunoreactivity of the CRF, somatostatin, and oxytocin systems showed no significant variation in either species. In contrast, in these two species, the immunoreactivity of the LHRH system varied considerably depending on the date of observation. The increase in the number and immunoreactivity of the LHRH-secreting neurons that occurred in November in the mink and in January in the ferret, is in agreement with previous results showing that the photoperiod plays an essential role in regulating the annual activity of the testis and that the photoperiodic environmental conditions required for the activation of the LHRH system differ between the species. Similarly, correlations could be found between an increase in immunoreactivity of the vasopressinergic axons projecting to the external median eminence and the recrudescence of testicular activity.
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PMID:Peptidergic neurohormonal systems in the basal hypothalamus of the ferret and the mink: immunocytochemical study of variations during the annual reproductive cycle. 334 34

The effects of colchicine on neurosecretory neurons of the rat hypothalamus were studied by immunocytochemistry, high-resolution radioautography, and conventional electron microscopy. In control rats, intraneuronal immunocytochemical labeling of vasopressin, oxytocin and somatostatin occurred essentially in the Golgi apparatus, the neurosecretory granules and to a lesser extent, the endoplasmic reticulum. These immunostaining patterns were dramatically modified 24 h after the administration of colchicine: immunoreactive peptides were located in granular or tubular structures accumulated at the periphery of the perikarya, but the Golgi stacks were not immunostained. Two h after the administration of tritiated leucine, quantitative analysis of radioautographic labeling of supraoptic perikarya revealed large amounts of radioactive protein in the Golgi saccules of neurosecretory neurons in control rats, but in the neurons of colchicine-treated rats, radioautographic labeling was mainly located in granular structures accumulated at the periphery of the perikarya, with no significant labeling on the Golgi stacks. Lastly, 3 noteworthy effects of colchicine on the ultrastructural morphological features of these neurosecretory neurons consisted in: (1) a dramatic disorganization of the Golgi complexes, (2) an accumulation of electron-dense proteic material within the lumen of cisternae of both the rough and smooth endoplasmic reticulum and, (3) a marked depolymerization of perikaryal microtubules, specifically those associated with the Golgi stacks. Taken together, these data do not fit the prevailing concept that the colchicine-induced accumulation of secretory material within the perikarya of neurosecretory neurons essentially results from the blockade of axoplasmic transport mechanisms. Instead, they support the idea that the effects of colchicine are related to the inhibition of the intraneuronal transport of newly synthesized secretory material from the endoplasmic reticulum to the Golgi apparatus, suggesting that the microtubules associated with the Golgi stacks are possible sites of colchicine action.
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PMID:Effects of colchicine on the intraneuronal transport of secretory material prior to the axon: a morphofunctional study in hypothalamic neurosecretory neurons of the rat. 340 58

Since neuroimmunomodulation is brought about in part, at least, by secretion of pituitary hormones involved in stress and immune responses, we review briefly the hypothalamic control of the release of ACTH, growth hormone, and prolactin. The release of ACTH is controlled particularly by corticotropin-releasing factor (CRF), but vasopressin has intrinsic releasing activity and potentiates the action of CRF at both hypothalamic and pituitary levels. Oxytocin may even potentiate the action of CRF, but has little, if any, ACTH-releasing activity by itself. In addition, epinephrine may augment responses to the CRFs. In contrast, growth hormone is under dual control by growth-hormone-releasing factor (GRF) and somatostatin, and prolactin is under multifactorial control by a series of inhibitors and stimulators. Dopamine is accepted as a physiological prolactin-inhibiting factor (PIF), but probably GABA and possibly acetylcholine as well are PIFs. There is good evidence for a peptide PIF as well. There are a number of prolactin-releasing factors (PRFs) which include oxytocin, vasoactive intestinal polypeptide, PHI and TRH. Several other peptides can also release prolactin, including angiotensin II. In response to stress there is a complex interaction of peptides intrahypothalamically. CRF augments its own release by an ultra short-loop positive feedback, and there is negative ultra short-loop feedback of GRF and somatostatin. Vasopressin appears to augment CRF release as well as to act directly on the pituitary, and there are complex interactions of various peptides to influence prolactin and GH release.
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PMID:The role of brain peptides in neuroimmunomodulation. 347 67

The effect of 15 defined neuropeptides on the mitogenic activation of lymphocytes from human thymus, guinea pig lymph nodes and rat spleen was investigated. Lymphocytes were incubated in the absence or presence of polyclonal T and B cell activators together with increasing doses of the neuropeptides, and harvested at 48 h of culture after pulse-labeling with 3H-thymidine to assess the DNA synthesis. A dose-related stimulatory effect on the spontaneous 3H-thymidine incorporation of human thymocytes was obtained with methionine-enkephalin (met-enk), motilin and neurotensin. Vasoactive intestinal polypeptide (VIP) and peptide HI (PHI) were inhibitory. A similar responsiveness was observed in cultures of phytohemagglutinin P (PHA)-activated human thymocytes. The low level of basal DNA synthesis of guinea pig lymph node cells was stimulated by VIP and inhibited by neuropeptide Y (NPY) and PHI. PHA-activated lymph node T lymphocytes were stimulated by neurotensin, bombesin and motilin, whereas NPY inhibited the thymidine uptake. The low rate of spontaneous DNA synthesis of rat spleen cells was increased in the presence of VIP. Met-enk stimulated both basal and dextran sulfate-activated splenic B cell proliferation, whereas PHI was inhibitory in both cases. The following peptides were found to be inactive in all the above assays: substance P, cholecystokinin-octapeptide, somatostatin, galanin, oxytocin, pentagastrin and gastrin-releasing peptide 1-27 and 14-27. Although the responses were generally of low magnitude and observed at high peptide concentrations, present study contributes to the understanding of possible mechanisms involved in interactions between the nervous and the immune system.
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PMID:Neuropeptide regulation of human thymocyte, guinea pig T lymphocyte and rat B lymphocyte mitogenesis. 349 94


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