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)

As part of a continuing investigation of the steric and electronic functions of the disulfide group in neurohypophyseal hormones on their biological activity, the synthesis of "oxytocin lactam", [cyclo-(1-aspartic acid,6-alpha,beta-diaminopropionic acid)]oxytocin, has been undertaken. The protected nonapeptide was prepared in a stepwise manner by solution techniques; after removal of side-chain protecting groups, formation of the briding amide bonds was accomplished by oxidation-reduction condensation. The analogue possesses rat uterotonic, avian vasodepressor, and rat antidiuretic potencies of 16 +/- 2, 6.6 +/- 0.6, and 5.6 +/- 3.8 units/mg, respectively.
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PMID:Replacement of the disulfide bond in oxytocin by an amide group. Synthesis and some biological properties of (cyclo-(1-L-aspartic acid,6-L-alpha,beta-diaminopropionic acid))oxytocin. 61 41

The effects of N-methyl-D-aspartic acid (NMDA), injected s.c. or i.p. in the dose range of 2.5-10 mg/kg, on oxytocin and vasopressin levels were assessed in conscious rats. NMDA administration was found to induce a dose-related increase in oxytocin concentration with a peak response at 7.5 min. Plasma vasopressin was elevated only after injection of the highest dose used (10 mg/kg). Thus, though at different thresholds, the release of both posterior pituitary hormones was stimulated after NMDA administration.
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PMID:N-methyl-D-aspartic acid injected peripherally stimulates oxytocin and vasopressin release. 147 91

Oxytocin, bradykinin, melittin and A23187 increased cyclic GMP levels through activation of soluble guanylate cyclase in cultured porcine kidney epithelial cells, LLC-PK1. NG-monomethyl-L-arginine, an inhibitor of endothelium-derived relaxing factor/nitric oxide formation, decreased both basal and stimulated levels of cyclic GMP in a concentration-dependent manner. L-Arginine, but not D-arginine, augmented basal as well as stimulated levels of cyclic GMP and prevented the inhibition induced by NG-monomethyl-L-arginine. Similar effects of L-arginine were also observed with L-argininamide, L-arginine ethyl ester, L-arginine methyl ester and the dipeptide L-arginyl-L-aspartic acid. NG-monomethyl-L-arginine did not affect cyclic GMP accumulation induced by sodium nitroprusside, an activator of soluble guanylate cyclase, and atrial natriuretic factor, an activator of particulate guanylate cyclase. Stimulatory effects of oxytocin, glyceryl trinitrate, sodium nitroprusside, bradykinin, melittin and A23187 on cyclic GMP accumulation were enhanced with superoxide dismutase and diminished with oxyhemoglobin. However, atrial natriuretic factor-induced cyclic GMP accumulation was not affected. Furthermore, endothelium derived relaxing factor-like activity was detected in the conditioned medium from LLC-PK1 cells stimulated with oxytocin. Based on these data, we conclude that endothelium-derived relaxing factor is produced in this cell type and participates in the regulatory mechanism of cyclic GMP formation as an intra- and intercellular messenger for activation of soluble guanylate cyclase.
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PMID:Formation of endothelium-derived relaxing factor in porcine kidney epithelial LLC-PK1 cells: an intra- and intercellular messenger for activation of soluble guanylate cyclase. 167 Oct 98

1. Recently it has been shown that injection of angiotensin II into the anterior diencephalon causes the rat to drink water. In the present experiments the dipsogenic action of a number of other substances including substances related to angiotensin was tested.2. Injection of 0.001 Goldblatt u. renin into the angiotensin-sensitive region causes the water-replete rat to drink. Drinking is slower in onset and continues for longer than after injection of angiotensin II.3. Synthetic tetradecapeptide renin substrate and angiotensin I were as effective as angiotensin II at causing water-replete rats to drink.4. beta-aspartic acid(1)-valine(5)-angiotensin II was also fully effective; but the D-arginine substituted octapeptide was much less effective.5. The (2-8) heptapeptide retained about 50% of the dipsogenic activity of the octapeptide, whereas the absence of phenylalanine at the other end of the peptide chain in the (1-7) heptapeptide results in an inactive compound.6. The (3-8) hexapeptide and the (4-8) pentapeptide, both of which have phenylalanine at the end of the chain, and the (1-4) and (5-8) tetrapeptide fragments of angiotensin II showed only a slight action on intake of water.7. Kallikrein, bradykinin, adenosine-3'5-cyclic phosphate, vasopressin and oxytocin caused no drinking when injected into the angiotensin-sensitive region.8. It is concluded that the requirements for the dipsogenic activity of angiotensin are the same as those for its other biological actions with the qualification that the precursor peptides are also active, presumably because they give rise to angiotensin II locally.
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PMID:The effect on drinking of peptide precursors and of shorter chain peptide fragments of angiotensin II injected into the rat's diencephalon. 432 62

Studies were carried out on the right auricle of the right atrium of two-day-old rats placed in a special chamber perfused with Ringer-Locke solution at room temperature. The contractions rate of the auricle was counted with the use of a stereomicroscope. The following amino acids dissolved in Ringer-Locke solution were tested: glycine, glutamic acid, serine, alanine, aspartic acid, gamma aminobutyric acid, leucine, and peptides: vasopressin and oxytocin. Glutamic acid in a concentration of 10(-1) mol/l induced a decrease in auricle contraction rate by 25%. Alanine in concentration 10(-2) mol/l induced a decrease by 22%. Leucine in concentration 10(-2) mol/l induced a decrease by 16% and in concentration ten times higher a decrease by 28%. The other tested amino acids, vasopressin and oxytocin in concentration used had no influence on the rate of contraction frequency of the isolated auricle.
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PMID:The influence of amino acids, vasopressin and oxytocin on spontaneous contraction of the right auricle of the right atrium of two-day-old rats in vitro. 654 86

Two human neurophysins have been purified from acetone-desiccated posterior pituitaries by acidic extraction, molecular sieving, and ion-exchange chromatography. The complete amino acid sequence of each protein has been determined by using a sequencer and characterizing two sets of overlapping enzymic peptides. The two neurophysins belong to two structural families previously defined as MSEL- and VLDV-neurophysins according to the nature of the residues in positions 2, 3, 6, and 7. (MSEL-neurophysins contain methionine-2, serine-3, glutamic acid-6, and leucine-7; VLDV-neurophysins contain valine-2, leucine-3, aspartic acid-6, and valine-7.) Human MSEL-neurophysin has only 93 residues instead of 95 usually found in MSEL-neurophysins from other mammalian species, probably because of a deletion of amino acids 91 and 92. Compared with bovine MSEL-neurophysin, nine variations (seven substitutions and two deletions) are observed. Human VLDV-neurophysin has 93 residues, as do the other mammalian VLDV-neurophysins. There are 11 substitutions when the comparison is made with bovine VLDV-neurophysin. Between the two human neurophysins, there are 26 variations. However, the central parts of the proteins (residues 10-70) are nearly identical. Furthermore, in this region identical substitutions are found in positions 29 and 60 of both neurophysins, suggesting either a single exon or some relationship between the two corresponding genes.
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PMID:Identification of human neurophysins: complete amino acid sequences of MSEL- and VLDV-neurophysins. 657 52

The effect of N-methyl-D-aspartic acid (NMDA), (+-)-alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA), or (+-)-trans-1-amino-1,3-cyclo-pentanedicarboxylic acid (ACPD) (5-60 ng in 0.3 microliter of saline) microinjected in the paraventricular nucleus of the hypothalamus on penile erection and yawning was studied in male rats. NMDA induced both penile erection and yawning in a dose-dependent manner. AMPA and ACPD also induced penile erection but less potently than NMDA, but were ineffective in causing yawning. NMDA effect on penile erection and yawning was prevented by (+)-MK-801 (0.05-0.1 mg/kg IP, 10 min before NMDA), by the oxytocin antagonist d(CH2)5Tyr(Me)-Orn8- vasotocin (50-100 ng ICV 10 min before NMDA), but not by haloperidol (0.1-0.5 mg/kg IP 10 min before NMDA). The results suggest that NMDA induces penile erection and yawning by increasing oxytocinergic transmission by acting in the paraventricular nucleus of the hypothalamus.
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PMID:Penile erection and yawning induced by paraventricular NMDA injection in male rats are mediated by oxytocin. 751 86

In order to shed some light on the neurotransmitters in the spinothalamic tract (STT), we examined, biochemically and immunohistochemically, the contents of various neurotransmitter candidates in the terminal field of the STT after cervical hemi-chordotomy (HC) and dorsal quadrant-chordotomy (dQC) in the rat. Substance P (SP), calcitonin gene-related peptide (CGRP), enkephalin, neuropeptide Y, neurotensin, oxytocin and dynorphin A were analyzed immunohistochemically. The contents of neuropeptides (SP, CGRP and cholecystokinin octapeptide) were measured by radioimmunoassay and those of amino acids (aspartic acid, glutamic acid, gamma-aminobutyric acid (GABA) and glycine) and noradrenaline were determined using high-performance liquid chromatography. Cervical hemi-chordotomy, but not dQC, caused significant decreases of the SP-like immunoreactivity in and SP content of the ventral thalamus on the ipsilateral side, compared with that on the contralateral side and of rats subjected to sham-operation. However, neither HC nor dQC resulted in any changes in the ventral thalamic contents of other putative neurotransmitters examined. These results suggest that, in rats, the STT contains SP and that SP-positive fibers run in the ventral half of the ascending spinal tract at the cervical level.
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PMID:Substance P is a possible neurotransmitter in the rat spinothalamic tract. 753 53

To examine whether an excitatory amino acid (EAA) neurotransmitter may influence the secretion of oxytocin (OT), agonists and antagonists selective for three major groups of EAA receptors were microinjected into the area of right supraoptic nucleus (SON) of conscious unrestrained lactating rats. An increase in plasma OT concentration was induced by the EAA receptor agonist R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainic acid, but not by agonists at other EAA receptors, such as N-methyl-D-aspartic acid (NMDA) or the metabotropic agonist (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid. Increasing AMPA doses between 0.1-0.8 nmol/SON progressively increased the percentage of animals showing OT discharges to 100% at the highest dose, whereas the responding animals showed similar elevations of plasma OT regardless of dose. OT release induced by intra-SON AMPA was prevented by treatment with the selective non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione, but not by antagonists of the NMDA receptor. Administration of this antagonist in the third ventricle blocked the release of OT and PRL induced by suckling. The L-type Ca2+ channel antagonist nimodipine and the Na+ channel inhibitor 3-amino-N-(aminoiminomethyl)5-(N-ethyl-N-isopropyl)6-chloropyra zinecarboxamide produced an additive blockade of AMPA-induced OT release, whereas the N-type Ca2+ channel-preferring antagonist omega-conotoxin GVIA had no effect. These findings suggest that an EAA, most likely glutamate, participates in the physiological regulation of OT release in the lactating rat via actions at an AMPA/kainate receptor subtype that gates Na+ and Ca2+.
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PMID:Stimulation of oxytocin release in the lactating rat by central excitatory amino acid mechanisms: evidence for specific involvement of R,S-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-sensitive glutamate receptors. 769 46

In order to evaluate a possible role of brain nitric oxide (NO) on the control of penile erection, the effect of nitroglycerin, that is thought to act by producing NO, was studied on spontaneous penile erection in male rats. In addition the effect of drugs that prevent NO formation and/or activity such as NG-nitro-L-arginine methyl ester (NAME) and methylene blue, on N-methyl-D-aspartic acid (NMDA)-, apomorphine- and oxytocin-induced penile erection was also studied. Nitroglycerin induced penile erection in a dose-dependent manner when given intracerebroventricularly (i.c.v.) (33-99 micrograms) or in the paraventricular nucleus of the hypothalamus (0.8-3.3 micrograms). Nitroglycerin-induced penile erection was prevented by the guanylate cyclase inhibitor methylene blue injected i.c.v. (200-400 micrograms) but not in the paraventricular nucleus of the hypothalamus (10-20 micrograms). Conversely, NMDA-, apomorphine- and oxytocin-induced penile erection was prevented by NAME (150 micrograms) or methylene blue (400 micrograms) given i.c.v. NAME (20 micrograms), but not methylene blue (20 micrograms), was effective in preventing the behavioral response also when injected in the paraventricular nucleus. The present results suggest that NO is a common mediator of several neurotransmitters involved in the control of this primary male sexual function.
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PMID:Nitric oxide is a central mediator of penile erection. 787 Feb 89


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