Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of methionine(met)-enkephalin, leucine(leu)-enkephalin, beta-endorphin and blocking substances upon renal function were studied in conscious goats. Injections were made through a permanent cannula into the 3rd ventricle. Leu- and met-enkaphalin, as well as beta-endorphin induced an antidiuretic response to the pituitary type. The responses to beta-endorphin were found to be dose-dependent. Pretreatment with naloxone, either into the 3rd ventricle or into the jugular vein, antagonised the antidiuretic responses to injected opioid peptides with the magnitude of the inhibition being dependent upon the dose. Atropine, hexamethonium or phentolamine did not interfere with the antidiuretic activity of beta-endorphin. Injection of naloxone alone into the 3rd ventricle of goats with a normal water balance, induced both a diuretic response and an increase in free water clearance. It is suggested that the opioid peptides are acting selectively on opiate receptors to influence the release of antidiuretic hormone.
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PMID:Effect of intracerebroventricular administration of opioid peptides on urinary function in the conscious goat. 737 1

The effects of beta-endorphin and various enkephalins on protein synthesis in eukaryotic cell-free systems have been examined. Beta-Endorphin, Leu-enkephalin, and Met-enkephalin inhibit the incorporation of radioactive leucine into globin in the presence of reticulocyte poly(A)+ RNA and of radioactive phenylalanine into polyphenylalanine in the presence of poly(U); however, the poly(U)-dependent synthesis of polyphenylalanine from Phe-tRNA is not inhibited. the aminoacylation of tRNAPhe is markedly inhibited by enkephalin, indicating that the sensitive component is Phe-tRNA synthetase. Other aminoacyl-tRNA synthetases are not significantly affected. The interaction between enkephalin and Phe-tRNA synthetase is reversible; activity is restored by dialysis of enzyme-enkephalin reaction mixtures. Morphine, vasopressin and analogues of vasopressin, and enkephalin analogues such as [D-Ala2,D-Leu5]enkephalin and [D-Ala2,Met]enkephalinamide have no effect on translation. The results suggest that the effects on protein synthesis are probably not related to opiate effects.
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PMID:The effects of beta-endorphin and enkephalins on protein biosynthesis in a eukaryotic cell-free system. Inhibition of phenylalanyl-tRNA synthetase. 744 May 77

Experiments were performed to study the effects of opioids on both the plasma arginine vasopressin and renal responses to hypertonic saline. Neither the opiate antagonist naloxone nor the enkephalin agonist DAMME [D-Ala2, MePhe4, Met (0)-ol)enkephalin] altered the vasopressin response to the same hypertonic stimulus, although DAMME increased free water clearance. In man, opioids do not seem to be important mediators of the vasopressin response to osmolar change.
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PMID:Effects of the opiate antagonist naloxone and the enkephalin analog DAMME on the vasopressin response to a hypertonic stimulus in man. 744 Jul 6

Radioimmunoassay of methionine-enkephalin, leucine-enkephalin and beta-endorphin were used in order to study the distribution and release of endorphins. The distribution pattern of enkephalin immunoreactivity in brain, including human brain, is quite different from that of beta-endorphin immunoreactivity. Separation of beta-endorphin and beta-lipotropin by column chromatography revealed that the contribution of beta-lipotropin to beta-endorphin immunoreactivity in brain is very small. In the anterior lobe of the pituitary both beta-endorphin and beta-lipotropin were found, whereas in the intermediate/posterior lobe almost all immunoreactivity was due to beta-endorphin; considerable amounts of enkephalin were also detected. Raising the concentration of potassium ions stimulated the release of met- and leu-enkephalin from striatal slices and the release of beta-endorphin immunoreactive material(s) from hypothalamic slices; both phenomena were dependent upon the presence of calcium ions. Studies of the release of beta-endorphin from isolated rat pituitaries revealed characteristic differences between the anterior and intermediate/posterior lobes; e.g., lysine vasopressin and extracts from the median eminence were highly effective in releasing beta-endorphin from the anterior lobe without affecting the release from the intermediate/posterior lobe; on the other hand, dopamine inhibited beta-endorphin release from the intermediate/posterior lobe without affecting release from the anterior lobe. Increased beta-endorphin levels were found after various stress conditions in rat plasma, as well as after treatment with metyrapone and vasopressin. In normal human plasma significant amounts of beta-endorphin were detected; increased levels were found in Addison's, Nelson's and Cushing's disease. Chronic opiate treatment of rats for 10 days did not affect brain levels of enkephalin or the beta-endorphin content of the hypothalamus, pituitary and plasma. Precipitated withdrawal decreased beta-endorphin in the anterior lobe and hypothalamus and increased beta-endorphin levels in the plasma. Long-term morphine treatment (30 days) decreased enkephalin and beta-endorphin content in some brain areas and in the intermediate/posterior pituitary lobe but not in the anterior lobe.
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PMID:Functional aspects of endorphins. 744 28

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (D-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.
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PMID:Increased pressor responsiveness to enkephalin in spontaneously hypertensive rats: the role of vasopressin. 744 62

Nine articles published since January 1992 on new methods of evaluating hepatic function are reviewed. These articles described the clinical significance of blood levels of cytokines, fibrin- or fibrinogen-related antigens, vitronectin, and endothelin, and of magnetic resonance spectroscopy, methionine metabolism, vasopressin clearance, vascular compliance, and radioreceptor imaging in gastroenterology. None of the methods have yet been applied to surgery. In addition, the redox theory, the evaluation of hepatic mitochondrial redox potential by arterial ketone body ratio and its clinical application, is introduced, and recent publications on the assessment of graft viability in liver transplantation and preoperative hepatic functional reserve in liver surgery based on the theory are reviewed.
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PMID:Evaluation of hepatic function. 758 58

The effect of human chorionic gonadotropin (hCG) on intact Leydig cell phospholipid methylation was studied. Hormonal stimulation of rat Leydig cells increased the incorporation of [methyl-3H]methionine into phospholipids threefold. This effect was observed after 10 minutes of incubation time and was time and dose dependent with a maximal stimulation at 67 ng/ml of hCG. In the presence of hCG, 3H-labeled methyl groups were preferentially incorporated into phosphatidyl-N-monomethylethanolamine. This effect of hCG was not reproduced by dibutyryl cyclic adenosine monophosphate (cAMP), cholera toxin, or forskolin. Purified hCG beta subunit but not hCG alpha subunit had stimulatory activity on Leydig cell phospholipid methylation. We conclude that luteinizing hormone (LH)/hCG stimulates specifically Leydig cell phospholipid methylation, because LH-releasing hormone or [Arg8]-vasopressin did not modify these reactions. We postulate that these reactions are occurring at a cellular level that involves hormone-receptor interaction. It is also suggested that this biological response involves hCG beta subunit receptor interaction and does not require cAMP synthesis.
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PMID:Human chorionic gonadotropin and free beta subunits stimulate phospholipid methylation in intact rat Leydig cells. 769 25

The secretion of oxytocin (OXT) from the neurohypophysis is modulated by the actions of opioids acting via kappa-receptors. The vasopressin (AVP)-containing nerve terminals in the neurohypophysis contain the kappa-opioid agonist dynorphin, but endogenous opioid restraint of OXT secretion is observed even when AVP release is not activated, suggesting that another source of opioids is responsible for modulating OXT secretion. We now report that acute stimulation of the rat neural lobe in vivo results in depletion of the neural lobe content of OXT, AVP, dynorphin A1-17, dynorphin A1-8 and metenkephalin (Met-Enk). The dynorphin content is depleted to a similar extent as that of OXT and AVP; a correlation analysis suggests that while most dynorphin is co-secreted with AVP, a significant portion is co-secreted with OXT, consistent with a co-localisation of dynorphin with OXT. Met-Enk was depleted to a lesser extent than either hormone, consistent with a partial localisation in non-releasable pools. However, depletion of Met-Enk was also observed following naloxone-precipitated opioid withdrawal accompanying selective hypersecretion of OXT, suggesting co-secretion of OXT and Met-Enk. Met-Enk is a mu-opioid receptor agonist, but extended forms of Met-Enk, as we now report, are active at neurohypophysial kappa-receptors.
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PMID:Stimulus-induced depletion of pro-enkephalins, oxytocin and vasopressin and pro-enkephalin interaction with posterior pituitary hormone release in vitro. 770 Apr 99

The localizations of peptides and putative neurotransmitters in the subfornical organ of the rabbit, rat and guinea pig were analyzed by using immunohistochemical methods. The variations that occurred in the three species were investigated. Immunoreactivities including serotonin (5-HT), neurotensin (NT), vasopressin (VP), luteinizing hormone releasing hormone (LHRH) and FMRFamide (Phe-Met-Arg-Phe-NH2) were examined in the subfornical organ. Nerve fibers that displayed 5-HT-positive immunoreactivity were observed in all species examined. Some immunoreactive perikarya were detected in guinea pigs and rabbits. Neurotensin-positive immunoreactivity was weak in the subfornical organ. LHRH immunoreactivity was detected in the rabbit only. Conspicuous vasopressin-positive immunoreactive cell bodies and fibers were detected in the subfornical organ of the rat, rabbit and guinea pig. Mild FMRFamide-positive immunoreactive fibers were observed in the rabbit and rat and no reaction was shown in the guinea pig by the PAP immunolabeling technique. Each neurotransmitter had a specific pattern of distribution in the SFO, though there were some overlapping reactive areas. Dramatic differences were demonstrated for fiber density among species.
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PMID:Immunohistochemical analysis of neurotransmitters of the subfornical organ. 770 63

The present study was conducted to visualize neuropeptides in the SCN of a mustelid, the American mink in which seasonal cycles of reproduction rely totally on the annual changes in day length. At this time, data in mustelids are lacking. Results were obtained with in situ hybridization (ISH) using synthetic oligonucleotide vasopressin (AVP) and somatostatin (SOM) and with single and dual immunohistochemistry (IHC) performed with antisera against AVP, SOM, vasoactive intestinal polypeptide (VIP), gastrin releasing peptide (GRP) and met-enkephalin (Met-ENK) in untreated (AVP and VIP) or colchicine (SOM, Met-ENK and GRP) treated adult male and female mink. The most striking result, evidenced by ISH as well as IHC was the lack of AVP, SOM and Met-ENK immunoreactive (ir)-neurons in the SCN. In contrast, strongly VIP ir-perikarya were widely distributed within the SCN and gave rise to a dense network of fibres extending within the periventricular (peVA) and subparaventricular (subPVA) areas. Weakly GRP ir-perikarya were also observed in the median part of the SCN. Dual IHC revealed that the magnocellular neurons located just dorsal to the SCN, in the peVA and subPVA co-stored AVP with VIP, SOM or Met-ENK. The lack of SCN AVP and SOM ir-neurons, reported for the first time in a mammalian species, raises the question of their implication in the functions of the circadian pacemaker and its entrainment by the light/dark cycle in other species. The significance of the large neurons co-storing peptides in the terminal field of VIPergic fibres originating in the SCN has also to be determined. These results suggest that VIP could be of major importance in processing photic information mediating circadian entrainment and consequently annual rhythms.
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PMID:Vasoactive intestinal polypeptide in the suprachiasmatic nucleus of the mink (Mustela vison) could play a key role in photic induction. 773


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