UNIPROT:P01178 - FACTA Search

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

The ability of centrally administered vasoactive intestinal peptide (VIP) to stimulate PRL secretion when injected intracerebroventricularly could be due to leakage to the pituitary, where it is known to exert direct PRL-releasing activity, or to a hypothalamic action on its own release or that of another possible PRL-releasing factor. When 3 micrograms VIP were injected into the third ventricle of conscious ovariectomized rats, a significant (P less than 0.005) and transient elevation of plasma oxytocin (OT) levels was observed. When OVX rats were injected iv with 1 ml anti-OT serum 30 min before the central administration of 3 micrograms VIP, the PRL surge seen after VIP injection in normal rabbit serum-treated controls was completely absent. The PRL surge seen after central VIP administration was not significantly altered by iv saline infusion (1 ml over 30 min) or by infusion of a VIP antagonist [D-4-Cl-Phe6,Leu17]VIP at a dose of 0.5 microgram/kg.min in 1 ml saline for 30 min before the VIP injection. This was not due to the inability of the VIP antagonist to block the PRL-releasing factor activity of VIP, since it significantly antagonized that action both in vitro and in vivo in the suckling stimulation paradigm. However, the PRL surge was completely absent in ovariectomized rats pretreated by iv infusion of an OT antagonist, [deamino Cys1,D-Trp2,Val4,Orn8]OT, at a similar dose. This recruitment of OT by VIP indicates that it may act at more than one locus within the hypothalamo-pituitary axis to insure the coordinated control of PRL secretion.
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PMID:Oxytocin mediates the hypothalamic action of vasoactive intestinal peptide to stimulate prolactin secretion. 291 3

We have reported that microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius of urethan-anesthetized normotensive rats produces an increase in mean arterial pressure (MAP) over the dose range 50-500 pmol. The effect in spontaneously hypertensive rats (SHR) is now reported. Over the range 100-500 pmol SHR exhibit increases in MAP and heart rate greater than Wistar-Kyoto or Sprague-Dawley rats. SHR did not exhibit exaggerated responses to intravenous phenylephrine, suggesting a central site of increased responsiveness to ANG II. We also found depressor effects in Sprague-Dawley at lower doses (0.1 and 1 pmol). The decreases in MAP were extremely variable and not dose related. A selected dose of additional neuropeptides identified in the NTS was tested. Somatostatin, bradykinin, and vasoactive intestinal peptide (0.5 nmol) were without cardiovascular effects. Oxytocin and vasopressin, however, produced significant increases in MAP. Substance P produced a very small but significant increase in heart rate and MAP. Interaction between the vasopressin and ANG II pressor effects was studied, and each proved to be independent.
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PMID:Neuropeptide action in nucleus tractus solitarius: angiotensin specificity and hypertensive rats. 293 Oct 31

Suspensions of rat anterior pituitary cells were exposed to corticotropin-releasing factor (CRF) (5 nM) and various neurohormones (0.002-1000 nM). CRF-induced secretion of ACTH was doubled by 0.1 nM arginine vasopressin (AVP), 0.2 nM arginine vasotocin, 1 nM oxytocin, 10 nM angiotensin II, and 100 nM noradrenalin; vasoactive intestinal peptide had no effect at 0.2-200 nM. CRF potentiation by AVP was also observed at lower concentrations of CRF. Since AVP appeared to be the most potent modulator of CRF-induced ACTH secretion, potentiation was further tested with specific antidiuretic and oxytocic agonists. Potentiation was clearly related to pressor biological activity, less so to antidiuretic, and hardly at all to oxytocic activities. However, even at 200 nM, the antipressor antagonists dPTyr(Me)AVP and d(CH2)5Tyr(Me)AVP had no effect on potentiation by AVP. The lack of antagonism was partly due to the agonistic effects of the antagonists on the pituitary gland, an effect not observed within vascular tissue. The results thus suggest that anterior pituitary vasopressin receptors resemble, but are not identical to, V1 (pressor and hepatic), do not resemble the V2 (renal), and might be classified as V3 (pituitary) receptors.
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PMID:A novel type of vasopressin receptor on anterior pituitary corticotrophs? 298 63

Neuropeptides and biogenic amines known to be present in neurons or afferent terminals in the paraventricular nucleus (PVH), supraoptic nucleus (SON) and/or lateral hypothalamus (LH) were added to small areas of these structures obtained by micropuncture and cyclic adenosine monophosphate (cAMP) levels were measured. cAMP accumulation occurred in PVH, SON and LH in response to neuropeptides of the secretin family, such as vasoactive intestinal peptide (VIP) and in response to catecholamines. Bradykinin, alpha-melanocyte-stimulating (alpha-MSH), luteinizing hormone-releasing hormone (LH-RH), oxytocin and carbamylcholine stimulated cAMP accumulation selectively in one or two of the above structures. Glucagon, cholecystokinin (CCK), somatostatin (SRIF), corticotropin-releasing factor (CRF), thyrotropin-releasing hormone (TRH), adrenocorticotropin (ACTH), melanocyte-stimulating hormone (MSH), methionine enkephalin (Met-Enk), beta-endorphin, neurotensin, bombesin and angiotensin II did not effect cAMP levels while leucine enkephalin (Leu-Enk), arginine vasopressin and gamma-aminobutyric acid (GABA) elicited regionally selective decreases in basal levels of cAMP. When interactions between some of these compounds were measured, VIP and norepinephrine exerted a more than additive effect on cAMP elevation in the PVH, while the effect on cAMP of the SON and LH was additive.
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PMID:Interaction of neuropeptides and biogenic amines on cyclic adenosine monophosphate accumulation in hypothalamic nuclei. 300 57

The aim of the present study was to investigate how suckling influences the plasma levels of oxytocin and vasoactive intestinal peptide in lactating dogs. Blood-samples were drawn from ten lactating beagles during suckling, in week one and week three of the five week long lactation period and the levels of vasoactive intestinal peptide and oxytocin were determined by radioimmunoassay. The immunoreactive levels of vasoactive intestinal peptide and oxytocin (below referred to VIP and oxytocin) increased rapidly in response to the suckling stimulus. The rise of both peptides was significant at both suckling experiments. The origin and role of suckling-released oxytocin is well established. The origin of and function of the VIP released in response to suckling remains unknown.
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PMID:Increased levels of vasoactive intestinal peptide (VIP) and oxytocin during suckling in lactating dogs. 365 10

The concentration of vasoactive intestinal peptide (VIP) was measured by RIA in pituitary extracts of female cats; it was significantly higher in the posterior than in the anterior lobe, 47.3 +/- 3.9 pmol/g wet wt vs. 7.7 +/- 2.0 pmol/g wet wt (mean +/- SE, n = 5 in both instances). To investigate the effect of VIP on the release of posterior pituitary hormones, the concentration of arginine vasopressin and oxytocin was measured by RIA in jugular vein plasma during intracarotid infusion of VIP. The levels of both hormones rose during the 5-min infusion of VIP. Oxytocin levels increased from a mean of 7.9 microU/ml to a maximum of 34.9 microU/ml at 1 min and arginine vasopressin levels from from 27.4 microU/ml to a maximum of 157 microU/ml at 1 min. The levels of both hormones returned to baseline values in about 20 min. Since VIP has been localized to the nerve terminals of the neurohypophysis, these data suggest that endogenous VIP may play a role as a neurotransmitter in the magnocellular hypothalmo-neurosecretory system.
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PMID:Vasoactive intestinal peptide (VIP) stimulates oxytocin and vasopressin release from the neurohypophyis. 647 4

An indirect immunofluorescence technique was used to study the peptidergic innervation of the thyroid gland in homozygous Brattleboro rats (DI) and normal Long-Evans rats (LE). The primary goal of this study was to determine whether the previously demonstrated decrease in thyroid responsiveness to TSH in DI might be due to an abnormality in the innervation of the thyroid. Thyroids from both types of rats were found to contain nerve fibers containing immunoreactivity for vasoactive intestinal peptide (VIP), substance P (SP), neuropeptide Y (NPY), and peptide HI (PHI). All four types of fibers were found in close association with both follicle cells and blood vessels. Well developed networks of fibers surrounding blood vessels were particularly apparent in the case of NPY. The density of fibers associated with follicle cells in DI was at least as great as that in LE in regard to SP, NPY, and PHI. Fibers containing VIP were found in greater abundance in DI than in LE. Additional studies revealed no evidence of thyroid fibers containing either somatostatin or neurophysin, which was used as a marker for vasopressin. We conclude that the reduced responsiveness of the thyroid in DI is not due to an inadequate supply of any of the neuropeptides included in this study. Since VIP is known to enhance thyroid secretion, we suggest that the apparent proliferation of VIP-containing fibers in DI may be a reflection of a neural mechanism attempting to compensate for a thyroid gland deficiency analogous to the humoral mechanism by which TSH secretion increases in response to thyroid deficiency.
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PMID:Immunocytochemical studies of the peptidergic innervation of the thyroid gland in the Brattleboro rat. 654 94

1. The action of vasoactive intestinal peptide (VIP) on the electrical and mechanical activity of strips of longitudinal myometrial smooth muscle from rabbits and guinea-pigs treated with oestradiol was studied in the sucrose-gap apparatus. 2. In myometrial strips which spontaneously exhibited regular contractions, or which were induced to contract rhythmically to the application of oxytocin, VIP reduced both the frequency and the force of contraction. 3. Contractions were associated with bursts of action potential discharge. In guinea-pig, the membrane potential reached its most negative value shortly following a burst and a slow decay of negativity followed ("generator potential'). VIP inhibited the decay of this negativity and increased the duration of the period between bursts. In rabbit myometrical strips, electrical discharges occurred less regularly but VIP also had an inhibitory action. The inhibitory action of VIP was not affected by the beta-adrenoreceptor blocker propranolol, by tetrodotoxin, or by apamin. 4. Using the double sucrose-gap apparatus, bursts of action potentials and contractions were elicited with depolarizing electrical pulses in the absence of oxytocin. Changes in membrane resistance were also estimated by eliciting hyperpolarizing electrotronic potentials. VIP hyperpolarized the membrane and inhibited contractions as depolarizing pulses now failed to reach threshold for action potential discharge or fewer action potentials were discharged. A small (about 10%) reduction in membrane resistance was freqeuently observed during the hyperpolarization. 5. If a single action potential was elicited in the presence of VIP, the tension generated by the muscle was less than in its absence. 6. In a calcium-free high-potassium (126 mM) solution, readmitting calcium produced contraction; VIP inhibited this contraction. Activation of beta-receptors by means of isoprenaline had a similar effect but unlike isoprenaline the action of VIP was not blocked by propranolol. 7. It is suggested that the primary action of VIP is on the calcium economy of the myometrial smooth muscle cell, possibly to accelerate sequestration and/or extrusion of calcium from the cell. In some way this is associated with inhibition of the generator potential, hyperpolarization, and with a small increase in permeability of the membrane to potassium.
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PMID:Mechanism of action of vasoactive intestinal polypeptide on myometrial smooth muscle of rabbit and guinea-pig. 732 Aug 97

The release of vasoactive intestinal peptide (VIP) from the canine gut and its possible neural origin were studied using two agents, oxytocin and neostigmine, known to increase peripheral levels of VIP. Oxytocin and neostigmine increased the portal concentrations of VIP by threefold and sevenfold, respectively. A considerable portal/femoral vein gradient ranging from twofold in the basal state to sevenfold during stimulation with neostigmine indicated that the gut was the main source of circulating VIP. The contribution of the brain was minor, and that of the uterus was undetectable. Release of VIP occurred from the entire gut: After enterectomy, the residual gut (stomach, pancreas, and proximal duodenum) released spontaneously a large amount of VIP which masked the effect of oxytocin. Tetrodotoxin and hexamethonium, but not atropine, inhibited oxytocin-stimulted release of VIP by 80% and 60% respectively. This prompted the conclusion that the release of VIP was predominantly neurally mediated and that the chain of transmission involved a preganglionic cholinergic pathway. Hexamethonium strongly inhibited neostigmine-stimulated release of VIP. Atropine was even more potent in that it abolished the effect of neostigmine. The effect of atropine was attributed to a blockade of ganglionic muscarinic receptors, which are preferentially activated by cholinesterase inhibitors like neostigmine. The results of this study and those derived from electrical stimulation of the vagus nerve are consistent with the hypothesis that circulating VIP is released from intrinsic neurons of the gut under preganglionic cholinergic control.
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PMID:Neural release of vasoactive intestinal peptide from the gut. 743 34

The viral transneuronal labeling method was used in combination with immunohistochemical procedures to identify CNS neuropeptide and monoamine neurons that innervate the sympathetic preganglionic neurons (SPNs) which project to the stellate ganglion--the principal source of the sympathetic supply to the heart. Transneuronal labeling was found at three CNS levels: spinal cord, brainstem, and hypothalamus. In the thoracic spinal cord, apart from the pseudorabies virus (PRV)-labeled stellate SPNs, PRV-labeled neurons were localized in laminae I/II, IV, V, VII, and X as well as in the lateral spinal nucleus and lateral funiculus. In the C1-C4 spinal segments, labeled neurons were found in the lateral funiculus as well as laminae V and VII of the spinal gray matter. PRV-labeled cells were identified in lamina V and the dorsolateral funiculus of the lumbar spinal cord. Three medullary areas were consistently labeled: rostral ventromedial medulla (RVMM), rostral ventrolateral medulla (RVLM), and caudal raphe nuclei. The greatest concentration of labeling was found in the RVMM. This projection arose from adrenergic, serotonergic (5-HT), thyrotropin releasing hormone (TRH), substance P, somatostatin, enkephalin, and vasoactive intestinal peptide (VIP) immunoreactive neurons. The RVLM projection originated mainly from C1 adrenergic neurons, some of which contained immunoreactive neuropeptide Y (NPY). C3 adrenergic-NPY neurons lying near the floor of the 4th ventricle were also labeled. Enkephalin-, somatostatin- and VIP-immunoreactive RVLM neurons also contributed to this projection. 5-HT neurons of the caudal raphe nuclei (raphe pallidus, raphe obscurus, and raphe magnus) were labeled; some of these contained substance P or TRH-immunoreactivity with an occasional neuron staining for all three putative neurotransmitters. In the pons, catecholamine neurons in the A5 cell group, subcoeruleus and Kolliker-Fuse nuclei were labeled. The midbrain contained relatively few infected cells, but some were present in the Edinger-Westphal and precommissural nuclei. Forebrain labeling was concentrated in the paraventricular hypothalamic nucleus (PVN) with lesser amounts in the lateral hypothalamic area (LHA) and the perifornical region. In the PVN, oxytocin-immunoreactive neurons accounted for the greatest chemically-defined projection while corticotrophin releasing factor (CRF), vasopressin-, and angiotensin II-immunoreactive neurons provided successively lesser inputs. In the LHA, angiotensin II-immunoreactive neurons were labeled. In summary, this study provides the first detailed map of the chemically-coded CNS neurons involved in the control of the cardiosympathetic outflow.
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PMID:Transneuronal labeling of CNS neuropeptide and monoamine neurons after pseudorabies virus injections into the stellate ganglion. 755 33

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