Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to gain better insight into the relationship between glucagon-like peptide-1 (GLP-1) (7-36) amide and vasopressin (AVP) and oxytocin (OX). In situ hybridization histochemistry revealed colocalization of the mRNAs for GLP-1 receptor, AVP, and OX in neurons of the hypothalamic supraoptic and paraventricular nuclei. To determine whether GLP-1(7-36)amide alters AVP and/or OX release, both in vivo and in vitro experimental study designs were used. In vivo, intravenous administration of 1 microg of GLP-1(7-36)amide into the jugular vein significantly decreased plasma AVP and OX concentrations. In vitro incubation of the neurohypophysis with either 0.1 or 1 microg of GLP-1(7-36)amide did not modify the release of AVP. However, addition of 1 microg of GLP-1(7-36)amide to the incubation medium increased slightly the secretion of OX. The coexpression of GLP-1 receptor and AVP mRNAs in hypothalamic supraoptic and paraventricular nuclei gives further support to the already reported central effects of GLP-1 (7-36)amide on AVP. Our findings also suggest a dual secretory response of AVP and OX to the effect of GLP-1 (7-36)amide, which most likely is related to the amount and/or the route of peptide administration.
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PMID:Coexpression of glucagon-like peptide-1 (GLP-1) receptor, vasopressin, and oxytocin mRNAs in neurons of the rat hypothalamic supraoptic and paraventricular nuclei: effect of GLP-1(7-36)amide on vasopressin and oxytocin release. 988 49

In the present series of experiments, we have examined the endocrine profile of two stable colonies of Sprague-Dawley rats, here labeled Stock A, and Stock B, differing markedly in their ability to acquire a conditioned avoidance response. On separate occasions, the animals were subjected to five daily sessions (approximately 20 trials per 15 min session) of conditioned avoidance training, measurements of startle reactivity to an auditory stimulation and open-field spontaneous locomotor activity observations. The experiments were concluded by taking blood samples for later analysis of plasma glucose and plasma levels of the following hormones: insulin, gastrin, CCK, glucagon, somatostatin, oxytocin and corticosterone. The low-performing Stock B animals were characterized by [1] being more reactive to sensory stimulation: higher startle amplitude and shorter startle latency; [2] having higher plasma insulin and corticosterone levels, whereas plasma gastrin and oxytocin were significantly lowered and a strong tendency for a decrease also in plasma CCK. There were no differences in spontaneous locomotor activity between the two substrains. Taking total variability in avoidance performance into account, there was a statistically significant positive correlation between plasma oxytocin, as well as gastrin, levels and avoidance performance. The evidence obtained here, and in other laboratories, suggests that the Stock B animals display hormonal changes indicative of a submissive-defensive reaction pattern. Thus, the avoidance acquisition deficits displayed by the present Sprague-Dawley stocks A and B, are in all probability caused by emotional reactions when challenged with external stimuli requiring active responding.
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PMID:Endocrine and behavioral traits in low-avoidance Sprague-Dawley rats. 1023 37

We characterized the receptors that mediate arginine vasopressin (AVP)- and oxytocin (OT)-induced glucagon release by use of a number of antagonists in the perfused rat pancreas and the fluorescence imaging of the receptors. AVP and OT (3 pM-3 nM) increased glucagon release in a concentration-dependent manner. The antagonist with potent V(1b) receptor-blocking activity, CL-4-84 (10 nM), abolished AVP (30 pM)-induced glucagon release but did not alter OT (30 pM)-induced glucagon release. d(CH(2))(5)[Tyr(Me)(2)]AVP (10 nM), a V(1a) receptor antagonist, and L-366,948 (10 nM), a highly specific OT-receptor antagonist, failed to inhibit AVP-induced glucagon release. In contrast, L-366,948 (10 nM) abolished OT (30 pM)-induced glucagon release but did not change the effect of AVP. Fluorescent microscopy of rat pancreatic sections showed that fluorescence-labeled AVP and OT bound to their receptors in the islets of Langerhans and that the bindings were inhibited by 1 microM of Cl-4-84 and L-366,948, respectively. Because AVP and OT at physiological concentrations (3-30 pM) increased glucagon release, we conclude that AVP and OT increase glucagon release under the physiological condition through the activation of V(1b) and OT receptors, respectively.
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PMID:Characterization of receptors mediating AVP- and OT-induced glucagon release from the rat pancreas. 1040 28

Glucagon-like peptide-1 (GLP-1) has been shown to bind to the posterior pituitary in the rat. We examined GLP-1 binding sites in human postmortem and rat pituitaries. Dense [125I]GLP-1 binding was seen in both human and rat posterior pituitary. In rat neurointermediate lobe membranes the binding site showed a Kd of 0.2 +/- 0.01 nM and a binding capacity of 600 +/- 33 fmol/mg protein (n = 3). In human pituitary membranes the binding site showed a Kd of 0.82 +/-0.05 nM and a binding capacity of 680 +/- 93 fmol/mg protein (n = 3). Chemical cross-linking showed a relative mol wt for the receptor-ligand complex of 73,100 +/- 1,400 (n = 3) in man and 59,300 +/- 900 (n = 3) in rat. GLP-1 (1 microM) failed to increase cAMP levels measured in rat neurointermediate lobes, whereas pituitary adenylate cyclase-activating polypeptide (100 nM) increased cAMP from a basal level of 14 +/-1 to 80 +/- 4 pmol/neurointermediate lobe 15 min (n = 5; P < 0.01). GLP-1 (up to 1 microM) did not affect the pituitary adenylate cyclase-activating polypeptide-stimulated cAMP levels. GLP-1 (up to 1 microM) also did not stimulate release of vasopressin or oxytocin from isolated rat neurointermediate lobes. The posterior pituitary shows the highest density of GLP-1-binding sites yet seen, but their function and signal transduction mechanism remain unknown.
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PMID:Characterization of human and rat glucagon-like peptide-1 receptors in the neurointermediate lobe: lack of coupling to either stimulation or inhibition of adenylyl cyclase. 1074 32

Bovine plasma was assayed to determine whether ergotamine, an ergopeptide isolated from endophytic tall fescue, affected cortisol, triiodothyronine, insulin, and glucagon concentrations. In Exp. 1, four heifers received an i.v. bolus injection of ergotamine tartrate (19 microg/kg BW) or saline vehicle in a simple crossover design 2 d after induced luteolysis. Oxytocin (100 USP units) was i.v. administered 4 h after ergotamine or saline. Treatment x time affected (P < .01) respiration rates and plasma concentrations of cortisol, triiodothyronine, insulin, and glucagon. Respiration rates were elevated (P < .01) 2 to 7 h after ergotamine, but they were unchanged after saline. Plasma cortisol concentrations were increased (P < .01) 1 to 3 h after ergotamine but not after saline. Plasma triiodothyronine was elevated 2 h after ergotamine, but it was unchanged in response to saline. Insulin decreased (P < .01) and glucagon increased (P < .01) during the 1st h after ergotamine, but not in response to saline. A second increase (P < .01) of glucagon was observed 3 h after ergotamine. In Exp. 2, six cows were treated with an i.v. bolus injection of ergotamine (20 microg/kg BW) or saline in a simple crossover design 10 d after receiving a s.c. ear implant containing norgestomet. Oxytocin (100 USP units) was i.v. administered 4 h after ergotamine or saline. Treatment x time affected (P < .001) respiration rates, cortisol, insulin, and glucagon and tended to influence (P = .12) triiodothyronine concentrations. Respiration rates were elevated (P < .01) 1 to 7 h after ergotamine but were unaltered by saline. Plasma cortisol was elevated (P < .01) 1 to 5 h after ergotamine, but not in response to saline. Plasma triiodothyronine was elevated (P < .01) 1 to 2 h after ergotamine, but not after saline. Insulin was decreased (P < .01) and glucagon increased (P < .01) within 1 h after ergotamine treatment, but they were not altered by saline. A second increase (P < .01) of glucagon occurred by 4 h after ergotamine. In Exp. 1 and 2, glucagon increased (P < .01) 1 h after oxytocin in saline and ergotamine cows. Results indicate that ergotamine can alter plasma concentrations of hormones that mediate nutrient metabolism and thermoregulation in cattle.
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PMID:Ergotamine alters plasma concentrations of glucagon, insulin, cortisol, and triiodothyronine in cows. 1076 77

The family of clinically available peptide hormones (PHs) is expanding in an exponential way, and advancement of knowledge of the basic mechanisms of action of PHs has led to multiplication of the possible clinical indications of already known PHs, and appears even more promising for still unknown PHs. A common obstacle to a full routine use of PHs is represented by the fact that PHs cannot be administered by the oral route, since they undergo digestion and inactivation in the gastrointestinal tract and a significant first pass metabolism in the liver. One alternative is represented by intranasal administration of PHs. The intranasal route of administration of PHs is also very attractive because of its convenience, which should assure a good compliance by patients. Luteinizing hormone releasing hormone, the analogues, desmopressin, oxytocin and salmon calcitonin are already marketed for intranasal administration; for salmon calcitonin, studies about bioavailability have been scanty in the past, but should be re-considered in order to fully explore its clinical benefit.Intranasal peptide hormones not yet on the market are insulin, glucagon, growth hormone releasing hormone (GHRH) and GHRP, GH and somatostatin, but the scenario is likely to change in a short period of time. Hexarelin seems very effective and is at a promising stage of development; also, glucagon appears mature enough to undergo extensive clinical evaluation and possibly marketing. The concern is why other peptides have not been further evaluated, as is the case for somatostatin and its analogues.
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PMID:Peptide hormones: Review of current and emerging uses by nasal delivery. 1083 81

The present study was designed to compare the effects of glucagon-like peptide-1 (7-36) amide (GLP-1) injected centrally or systemically in a dose range of 10-10000 ng on the vasopressin and oxytocin release as well as the blood pressure in the rat. The urethane-anaesthetised Wistar male and female rats were fitted with venous as well as arterial catheters and, in the second study, additionally with the intracerebroventricular cannula. The arterial blood pressure was monitored throughout the experiment. The plasma vasopressin/oxytocin concentrations were measured in blood samples taken 15 min before and 5, 15 and 30 min after the intravenous or intracerebroventricular GLP-1 injection. No gender-dependent differences were seen as to the GLP-1 effect on the blood pressure or the hormone release. GLP-1 administered centrally or systemically at low doses (10 or 100 ng) either showed a hypertensive or biphasic (an increase followed by a decrease in the blood pressure) effect. On the other hand, 1000 or 10000 ng GLP-1 caused a clear increase of the blood pressure regarding the way of injection. When injected systemically, GLP-1 increased the release of both neurohypophysial hormones. When injected centrally, however, GLP-1 either enhanced or, at low doses, significantly reduced the plasma vasopressin/oxytocin levels. The effect on the blood pressure seems to be independent of the possible pressor effect of endogenous vasopressin. It is concluded that GLP-1 may modulate the function of the hypothalamo-neurohypophysial system as well as the cardiovascular system through both the central and systemic mechanisms.
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PMID:Effects of centrally or systemically injected glucagon-like peptide-1 (7-36) amide on release of neurohypophysial hormones and blood pressure in the rat. 1096 3

With using pharmacological analysis of stimulation or blockage of enterocytes cholin- or adrenergic receptors chronic experiments on dogs with gastric fistulas were carried out to study the influence of peptides on gastric acid secretion stimulated by pentagastrin or histamine. The different peptides (met- and leu-enkephalins, substance P, angiotensins I and II, oxytocin, pentagastrin) and internal secretion hormones (insulin, glucagon) were infused parenterally under the stimulated gastric secretion. It is proposed the model of the peripheral link of neurohumoral regulation of gastric acid secretion in the stomach.
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PMID:[The role of peptides in the cholinergic and adrenergic mechanisms of the regulation of gastric secretion]. 1099 94

Neurohypophysial hormone receptors and second messengers were studied in trout (Oncorhynchus mykiss) hepatocytes. Arginine vasotocin (AVT) and isotocin (IT) elicited a concentration-dependent inhibition of cAMP accumulation in the presence of 5x10(-8) M glucagon (maximal effect for 4.5x10(-7) M and 1.4x10(-7) M, half-maximal effect for 2.1x10(-8) M and 0.7x10(-8) M, AVT and IT respectively). The effect of glucagon was inhibited up to 90% by AVT and 80% by IT. While AVT inhibited (up to 50%) the basal cAMP production, IT had no such action. Specific V(1) or V(2) analogues (with reference to vasopressin in mammals) were used for pharmacological characterization of the type of neurohypophysial hormone receptor involved in this inhibition. The V(1) agonist [Phe(2), Orn(8)]-oxytocin inhibited the glucagon-stimulated cAMP production with a maximal effect for 6x10(-7) M and a half-maximal effect for 0.9x10(-8) M concentrations of the analogue. While the V(1) agonist reduced the glucagon-stimulated cAMP level by 70%, it showed only a tendency to reduce the basal level. The V(2) agonist [deamino(1), Val(4),d -Arg(8)]-vasopressin had no effect either on basal or on glucagon-stimulated cAMP production. The V(1) antagonist [d(CH(2))(5)(1), O-Me-Tyr(2), Arg(8)]-vasopressin totally reversed the 10(-8) M AVT-induced inhibition of 5x10(-8) M glucagon-stimulated cAMP production, whereas the V(2) antagonist [d(CH(2))(5)(1),d -Ile(2), Ile(4), Arg(8), Ala(9)]-vasopressin had no such effect. In this particular case, maximal and half-maximal effects of the V(1) antagonist were obtained for 2.3x10(-6) M and 1. 2x10(-6 )M respectively. Changes in intracellular calcium content were measured using the fluorescent probe FURA-2/AM. AVT and IT elicited a concentration-dependent increase in Ca(2+) accumulation. The comparison of the effect of 10(-8) M agonists versus AVT showed the following order of potency: AVT=IT>V(1) agonist>V(2) agonist. The V(1) antagonist reversed the AVT-induced Ca(2+) accumulation whereas the V(2) antagonist had no such effect. These results are taken as evidence for the presence in trout hepatocytes of neurohypophysial hormone receptors functionally close to the V(1a)-type linked to cAMP production and Ca(2+) mobilization.
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PMID:Neurohypophysial hormone receptors and second messengers in trout hepatocytes. 1101 61

The innervation of the Brockmann bodies in the teleost fish, Blennius gattoruggine, was studied using immunocytochemical techniques at both the light and electron microscopy levels. Islet innervation consisted of intrapancreatic ganglia, generally localized inside the rim of the exocrine tissue of the Brockmann bodies, in proximity to the islet, nerve fibres and nerve terminals with synaptic complexes. The intrapancreatic ganglia were of variable size, with different numbers of ganglionic cells, that appeared unipolar in section. The cell bodies showed immunoreactivity to galanin, oxytocin, peptide tyrosine tyrosine and glucagon. The extrinsic and intrinsic nerve fibres passed through the exocrine parenchyma and crossed the connectival septa and islet connectival sheath, penetrating into the islets, where they became increasingly thinner. They terminated on the endocrine cells with dilated nerve terminals. At least three types of terminals were detected, depending on the different vesicle content: peptidergic, cholinergic or adrenergic. They presented specialized synaptic structures, the neuroglandular junctions, some of which contained neurosecretory granules immunogold labelled by galanin antiserum. This new finding confirms the role of galanin as a neurotransmitter. This rich supply of innervation may be important in the regulation and integration of islet secretion.
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PMID:An immunocytochemical study of intrapancreatic ganglia, nerve fibres and neuroglandular junctions in Brockmann bodies of the tompot blenny (Blennius gattoruggine), a marine teleost. 1120 57


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