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)

1. Intracellular recordings were made from identified and non-identified neurons in perioesophageal ganglionic ring with buccal ganglia of the mollusc, Helix pomatia. The influence of oxytocin (OXT) on neuronal integration: space and temporal summations of postsynaptic potentials (PSPs) in various neurons was investigated. The obtained data indicated that these PSPs were cholinergic PSPs. 2. Ten minute exposure to 10(-8) M OXT had no effects on the resting membranes, but triggered secondary mechanisms, which lead to enhancement of the excitatory PSP (EPSR) amplitudes and the decrease of the decay time constant (tau EPSR) obtained from the falling phase of the EPSP. 3. The enhancement of the EPSP amplitude and the decrease of tau EPSP after OXT application evoked the appearance of action potential under space summation of two spontaneous EPSPs and made easier the appearance of action potential under temporal summation of EPSPs produced by paired afferent stimuli, when the corresponding interstimuli interval was smaller than tau EPSP in the presence of OXT. 4. Ten minute exposure to 10(-8) M OXT made the integrated amplitude of the excitatory acetylcholine response and the inhibitory dopamine response in the neuron E5 more positive only when the interval between applications of these mediators was smaller than the time constant of desensitization of acetylcholine receptors in the presence of OXT. 5. The pharmacological studies showed that drugs, which elevate intracellular cyclic AMP levels, mimicked the influence of OXT on integration of PSPs in the investigated neurons.
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PMID:Influence of oxytocin on integration of postsynaptic potentials in molluscan neurons. 171 90

It was found that 10(-7)-10(-8) mol/l oxytocin (OT) or arginine-vasopressin (AVP) applications produced effects on functional properties of three types of acetylcholine (ACh) receptors on various neurons identified in the ganglia of Helix pomatia under voltage clamp conditions. OT and AVP depressed ACh-induced sodium-potassium-calcium current in neuron RBc3 without shift of reversal potential. Our data show that there are two types (subtypes) of ACh receptors which are connected with chloride current in neurons of Helix pomatia. OT decreased ACh-induced chloride current in neuron D4 and enhanced ACh-induced chloride current in neuron D5. These effects of OT were mimicked by the intracellular injection of cyclic AMP or application of isobutylmethylxanthine and an active cyclic AMP analog. AVP as a rule mimicked the effects of OT on functional properties of ACh receptors, but in neuron F8 effects of OT and AVP were independent. The present results suggest that cyclic AMP may be the second messenger mediating the OT- and AVP-induced modulations of functional properties of three types of ACh-receptors.
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PMID:Modulatory effect of oxytocin and arginine-vasopressin on functional properties of three types of acetylcholine receptors in molluscan neurons. 171 16

Administration (ip) into fed mice of glucagon, epinephrine, vasopressin, oxytocin, angiotensin II, and dibutyryl cyclic AMP (dbcAMP) resulted in a rapid (within 2.5 to 15 min) elevation of PRPP content (two- to threefold) and in acceleration of the rate of de novo purine synthesis (twofold). Inhibition of the epinephrine-stimulated glycogenolysis by 2,5-anhydromannitol diminished markedly the acceleration effect of the hormone on the rate of purine synthesis. Administration of the hormones caused a rapid rise in the liver content of glucose 6-phosphate (G6P) by 15-70% but did not increase the ribose 5-phosphate (R5P) content. Liver ATP content was not affected. The hormones did not cause direct activation of PRPP synthetase, as gauged by the specific activity of the enzyme, its Km for substrates R5P and ATP, and its sensitivity to inhibition by ADP and GDP. The hormones did not increase the liver content of the enzyme activators Pi and Mg2+. The results suggest that the glycogenolytic hormones accelerate purine synthesis by a metabolic mechanism associated with the enhancement of glycogenolysis. PRPP synthesis is probably enhanced by the glycogenolysis-induced alterations in the cellular content of some metabolites other than R5P.
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PMID:Acceleration of purine synthesis in mouse liver by glycogenolytic hormones. 172 6

We have measured the effects of oxytocin and three other compounds (chlorophenyl-thio-cyclic AMP, forskolin and theophylline) that increase cytoplasmic cyclic AMP on the impedance of the toad urinary bladder. Membrane capacitance was calculated from transepithelial impedance measured by a computerized sine wave method. All four agents increased tissue capacitance. Since in these tissues this parameter is proportional to apical membrane area our results suggest that cAMP can be a second messenger involved in the action of agents that promote fusion of exocytotic vesicles with the apical membrane.
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PMID:Cyclic AMP increases electrical capacitance of apical membrane of toad urinary bladder. 172 41

It was found that acetylcholine (ACh) at the concentration of 10(-3) M inhibited ADH-stimulated water transport through the wall of amphibian urinary bladder. This effect was suggested to be caused by an interaction of ACh with acetylcholinesterase (AChE) rather than by a stimulation of the M- or N-cholinoreceptor. The inhibitory action of ACh was completely suppressed in the presence of various AChE inhibitors (physostigmine, proserine, armine, Gd-42, acridine-iodmethylate), while an inhibitor of butyrylcholinesterase (BuChE), AD-4, failed to affect it. In accord with this observation the activity of AChE (but not of BuChE) was demonstrated in the urinary bladder epithelium. Since, in addition to the hydrosmotic effects of pituitrine, 8-arginine-vasopressin or oxytocin, ACh blocked also effects of forskolin or cyclic AMP, one may conclude that it acts at some post-cyclic AMP production stage. AChE-dependent inhibition of the ADH-stimulated water transport decreased significantly when the serosal pH was raising from 7.2 to 8.0, but was augmented by serosal acidification (pH 6.8), whereas such pH alterations did not affect the activity of the epithelium AChE. The effect of ACh under consideration was suppressed by adding amiloride (10(-4) M) to the serosal solution. Similarly, the ACh effect was blocked by an inhibitor of Ca-dependent K+ channels, 4-aminopyrdine, which in addition prevented the inhibition of the ADH-stimulated water transport by the serosal acidification. It was noteworthy that some other K+ channel blockers (Ba2+, Cs+, tetraethylammonium, apamine, quinine) did not affect either the water transport or the antipituitrine effect of ACh. In conclusion, we suggest that the inhibitory action of ACh on the ADH-stimulated water transport in the urinary bladder is mediated through the intracellular acidification resulting from ACh interaction with AChE. It is unlikely that the acidification is merely a consequence of the ACh hydrolysis, rather the ACh-AChE interaction induces directly an increase in the proton conductivity of the basolateral membrane of the urinary bladder epithelium.
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PMID:[Acetylcholinesterase and the ADH-dependent transport of water in the amphibian bladder]. 181 71

The effect of protein kinase C activation and dibutyryl cyclic AMP on oxytocin secretion by ovine luteal tissue slices was investigated. Several putative regulators of luteal oxytocin secretion were also examined. Oxytocin was secreted by luteal tissue slices at a basal rate of 234.4 +/- 32.8 pmol/g per h (n = 24) during 60-min incubations. Activators of protein kinase C: phorbol 12, 13-dibutyrate (n = 8), phorbol 12-myristate, 13-acetate (n = 4) and 1,2-didecanoylglycerol (n = 5), caused a dose-dependent stimulation of oxytocin secretion in the presence of a calcium ionophore (A23187; 0.2 mumol/l). Phospholipase C (PLC; 50-250 units/l) also caused a dose-dependent stimulation of oxytocin secretion by luteal slices. Phospholipase C-stimulated oxytocin secretion was potentiated by the addition of an inhibitor of diacylglycerol kinase (R59 022; n = 4). These data suggest that the activation of protein kinase C has a role in the stimulation of luteal oxytocin secretion. The results are also consistent with the involvement of protein kinase C in PLC-stimulated oxytocin secretion. The cyclic AMP second messenger system does not appear to be involved in the control of oxytocin secretion by the corpus luteum.
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PMID:Regulation of oxytocin secretion by the ovine corpus luteum: effect of activators of protein kinase C. 215 85

Release of oxytocin by sliced or minced sheep luteal tissue in vitro was stimulated up to 1.6- and 2.3-fold by arachidonic acid and the calcium ionophore A23187 respectively. Prostaglandin (PG) F2 alpha and the PGF2 alpha analogue cloprostenol, and other potential agonists known to be active in vivo, including noradrenaline and acetylcholine, were ineffective, as was the phorbol ester tetradecanoylphorbol acetate (TPA). The ineffectiveness of PGF2 alpha was not due to a general unresponsiveness of the tissue in vitro, as PGF2 alpha reduced LH stimulation of tissue concentrations of cyclic AMP and activated inositol lipid hydrolysis. The effect of arachidonic acid was accompanied by release from the tissue of the cytosolic enzyme lactate dehydrogenase (at arachidonic acid concentrations below those required to release oxytocin) and its effect on oxytocin and lactate dehydrogenase release was mimicked by oleic and linolenic acids; arachidonic acid was concluded to act by a non-physiological physicochemical effect without conversion to an eicosanoid. As PGF2 alpha in vitro is known to raise intracellular Ca2+ concentrations in the large luteal cells that secrete oxytocin, and as A23187 stimulates oxytocin release in vitro in the presence and absence of TPA, it is concluded that in-vitro incubation results in an artifactual blockade of the oxytocin-releasing action of PGF2 alpha at an unidentified point distal to the effect on intracellular Ca2+.
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PMID:Effects of prostaglandin F2 alpha and other potential secretagogues on oxytocin secretion and second messenger metabolism in the ovine corpus luteum in vitro. 216 27

Addition of vasopressin to hypothalamo-neurohypophysial explants in vitro increased cyclic AMP accumulation whereas exogenous oxytocin decreased cyclic AMP. An opposite response pattern was observed in the neural lobe of the pituitary where vasopressin decreased and oxytocin increased cyclic AMP accumulation. Forskolin elicited a 3-fold greater increase in cyclic AMP in the neural lobe than in the supraoptic nucleus and enhanced the sensitivity of the tissues to both vasopressin and oxytocin. The ability of both vasopressin and oxytocin to modulate local cyclic AMP metabolism suggests the possibility of internal feedback within the hypothalamo-neurohypophysial system.
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PMID:Vasopressin and oxytocin regulation of cyclic AMP accumulation in rat hypothalamo-neurohypophysial explants in vitro. 216 30

The response to small peptides such as Arg-vasopressin, oxytocin and tachykinins was investigated in cultured porcine aortic endothelial cells. The production of endothelium-derived nitric oxide was assessed indirectly by the accumulation of cyclic GMP, a response that is due to the increased activity of soluble guanylate cyclase of the endothelial cells after release of the mediator. Arg-vasopressin, oxytocin, substance P and physalae-min (an analog of substance P, pGlu-Ala-Asp-Pro-Asn-Lys-Phe-Tyr-Gly-Leu-Met-NH2) markedly and transiently stimulated the production of cyclic GMP without affecting that of cyclic AMP. Treatment of endothelial cells with either hemoglobin or methylene blue reduced significantly both the basal and stimulated level of cyclic GMP. The production of cyclic GMP evoked by Arg-vasopressin and substance P was inhibited selectively by NG-monomethyl-L-arginine but not by its D-enantiomer. The neurohypophyseal hormones and related peptides stimulated the accumulation of cyclic GMP in a concentration-dependent manner, with the following relative order of potency: oxytocin greater than Lys-vasopressin greater than Arg-vasopressin much greater than [deamino-Cys1, D-Arg8]-vasopressin. The production of cyclic GMP evoked by oxytocin was inhibited selectively by [d(CH2)5, Tyr(OMe)2, Orn8]-vasotocin, an oxytocin antagonist. The production of cyclic GMP evoked by Arg-vasopressin and Lys-vasopressin was inhibited by [beta-mercapto-beta, beta-cyclopentamethylene-propionyl1, O-Me-Tyr2, Arg8]-vasopressin, a selective V1-receptor antagonist. The moderate production of cyclic GMP evoked by [deamino-Cys1, D-Arg8]-vasopressin was inhibited significantly by the V1-receptor antagonist. The peptide antagonists affected only minimally or not at all the production of cyclic GMP evoked by a donor of nitric oxide, SIN-1 (3-Morpholino-Sydnonimine). These observations indicate that 1) neurohypophyseal hormones and tachykinins stimulate the accumulation of cyclic GMP in cultured porcine aortic endothelial cells by increasing the production of endothelial-derived nitric oxide, which in turn enhances the activity of soluble guanylate cyclase; 2) the production of cyclic GMP in response to oxytocin is due to activation of oxytocinergic receptors; and 3) the production of cyclic GMP evoked by Arg-vasopressin and Lys-vasopressin is due mostly to activation of V1-vasopressinergic receptors.
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PMID:Neurohypophyseal peptides and tachykinins stimulate the production of cyclic GMP in cultured porcine aortic endothelial cells. 217 9

It was found that 10(-8) mol/l oxytocin (OT) application exerted effects on functional properties of three types of acetylcholine (ACh) receptors in neurons identified in the ganglia of Helix pomatia under voltage clamp conditions. OT depressed ACh-induced sodium-potassium-calcium current in neuron RB3 without a shift of the reversion potential. The data obtained show that there are two types (subtypes) of ACh receptors connected with chloride channels. OT decreased the ACh-induced chloride current in neuron F4 and enhanced the ACh-induced chloride current and desensitization of ACh receptors in neurons D5, F86. Effects of OT and serotonin applications were reversible but not additional. Effects of OT injection and OT application were independent. The present results suggest that cyclic AMP may be the second messenger mediating the OT-induced modulation of functional properties of three types of ACh receptors.
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PMID:[Oxytocin modulation of the functional properties of 3 types of cholinoreceptors in mollusk neurons]. 233 36


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