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)

Intracerebral injections of puromycin one day after training of mice in a Y-maze cause amnesia when the animals are tested 7 days later. This amnesia was shown to be attenuated by various neurohypophyseal hormones, analogs and fragments, administered subcutaneously immediately after training. Dose-response relationships have been obtained for the attenuation of puromycin-induced amnesia in mice by selected neurohypophyseal peptides. All of the compounds tested reduce the amnesia in a dose-related way, suggesting that these peptides may interact with specific receptors to induce their central effect. Among the peptides studied the two most potent--i.e., those that cause substantial retention of memory at the lowest doses--are the neurohypophyseal hormone arginine vasopressin and Z-prolyl-leucyl-glycinamide (Z-MIF).
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PMID:Dose-response relationships in attenuation of puromycin-induced amnesia by neurohypophyseal peptides. 56 19

The reaction products of plasma enzyme degradation of TRH were identified by thin layer chromatography. The enzyme in normal rat plasma yields proline and pGlu-His as major reaction products. High concentrations of proline decrease peptide cleavage, resulting in greater amounts of acid TRH. The apparent Km of the enzyme is 4.1 X 10(-6) M. LHRH and neurotensin are competitive inhibitors with Ki of 5 X 10(-6) M and 1.5 X 10(-5) M, respectively. Somatostatin, MIF, oxytocin, arg-vasopressin, arg-vasotocin, neurophysin II and glucagon do not compete; and pGlu-His-Pro-OH, Glu-His-Pro-OH, pGlu-His, His-Pro-NH2, and Pro-NH2 do not affect enzyme activity. These data suggest that the substrated requires pGlu and a terminal or internal amide to complex with the enzyme. The enzyme is markedly inhibited by Cu++, Bal, benzamadine, p-(chloromercuri)-benzoic acid, moderately affected by EDTA and puromycin, and unaffected by mercaptoethanol. TSH does not affect enzyme activity while LH inhibits it moderately at high concentrations (300-600 pg/ml).
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PMID:Characteristics of the plasma TRH-degrading enzyme. 81 19

The effects of peptides on brain function suggest therapeutic and pathologic roles for these substances. Many peptides cross the blood-brain barrier (BBB) by transmembrane diffusion as a function of their lipid solubilities. Other peptides, such as the enkephalins, Tyr-MIF-1, vasopressin-related peptides, and peptide T-like peptides, are transported by carrier-mediated systems. Passage is influenced by aging, stress, lighting, drugs, amino acids, and neurotoxins. Disruption of the BBB results in complex changes in the blood and CSF levels of peptides. Peptides influence the passage of glucose, amino acids, and inorganic acids and may affect the integrity of the BBB. Peptide-BBB interactions have been suggested to play direct roles in dialysis dementia and maple syrup urine disease; they may be expected to be involved in other disorders of the CNS.
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PMID:Interactions between the blood-brain barrier and endogenous peptides: emerging clinical implications. 328 19

Peptides can be transported across the blood-brain barrier by saturable transport systems. One system, characterized with radioactively labeled Tyr-MIF-1 (Tyr-Pro-Leu-Gly-amide), is specific for some of the small peptides with an N-terminal tyrosine, including Tyr-MIF-1, the enkephalins, beta-casomorphin, and dynorphin (1-8). Another separate system transports vasopressin-like peptides. The choroid plexus has at least one system distinguishable from those above that is capable of uptake and possibly transport of opiate-like peptides. The possibility of saturable transport of other peptides has been investigated to a varying degree. Specificity, stereo-specificity, saturability, allosteric regulation, modulation by physiologic and pharmacologic manipulations, and noncompetitive inhibition have been demonstrated to occur in peptide transport systems and suggest a role for them in physiology and disease.
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PMID:Saturable transport of peptides across the blood-brain barrier. 330 36

A tabular synopsis is presented for articles concerned with the effects of peptides on the central nervous system that appeared in the journal Peptides from 1980-1985. A table arranged alphabetically by peptide and one arranged by effects, both listing routes of injection, species, direction of change, and qualifying notes, provides easy cross-referencing of peptides and their effects. Over 80 peptides and over 135 effects are listed. The list of peptides includes, but is not limited to: ACTH, angiotensin, bombesin, bradykinin, calcitonin, casomorphin, CCK, ceruletide, CGRP, CRF, dermorphin, DSIP, dynorphin, endorphins, enkephalins, GRF, gastrin, LHRH, litorin, metkephamid, MIF-l, motilin, MSH, NPY, NT, oxytocin, ranatensin, sauvagine, substances P and K, somatostatin, TRH, VIP, vasopressin, and vasotocin. The list of effects includes, but is not limited to: aggression, alcohol, analgesia, attention, avoidance, behavior, cardiovascular regulation, catalepsy, conditioned behavior, convulsions, dopamine binding and metabolism, discrimination, drinking, EEG, exploration, feeding, fever, gastric secretion, GI motility, grooming, learning, locomotor behavior, mating, memory, neuronal activity, open field, operant behavior, rearing, respiration, satiety, scratching, seizure, sleep, stereotypy, temperature, thermoregulation and tolerance.
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PMID:Central nervous system effects of peptides, 1980-1985: a cross-listing of peptides and their central actions from the first six years of the journal Peptides. 353 8

A brain to blood carrier-mediated transport system for arginine vasopressin (AVP) was investigated in mice after intraventricular injection of iodinated AVP and varying amounts of unlabeled material or candidate inhibitors. Residual activity in the brain detected after decapitation was used as the main determinant of transport activity. The half-time disappearance of iodinated AVP from the brain was 12.4 min, the Vmax was 1.41 nmol/g-min, and the apparent Km was 28.7 nmol/g. A 30-nmol dose of AVP, mesotocin, arginine vasotocin, pressinoic amide, pressinoic acid, tocinoic acid, and lysine vasotocin, but not oxytocin, lysine vasopressin, AVP free acid, tocinoic amide, Tyr-MIF-1, or cyclo Leu-Gly, significantly (P less than 0.05) inhibited the transport of iodinated AVP out of the brain. The 30 nmol dose of AVP had no effect on the transport of iodide or iodotyrosine out of the brain. High-performance liquid chromatography showed that 59.2% of the radioactivity found in the blood 2 min after an i.c.v. injection of labeled AVP eluted at the same position as labeled AVP compared with 68.8% of radioactivity eluting at that position after material was infused i.v. for 2 min. This indicates that intact peptide is transported across the blood-brain barrier and that most of the degradation of AVP occurs during circulation in the blood. Calculations based on the appearance of radioactivity in the periphery showed that 56.2% of the material injected centrally would have been transported into the periphery by 10 min. This appearance of material in the periphery was inhibited by the simultaneous injection of an excess of unlabeled peptide. Water loading significantly decreased the brain to blood transport rate of AVP by 40%. It is concluded that a saturable system exists for brain to blood transport of AVP and some structurally similar peptides.
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PMID:Carrier-mediated transport of vasopressin across the blood-brain barrier of the mouse. 369 15

Opioid analgesics influence the function of a number of neurotransmitter systems including classical neurotransmitters, neuropeptides and endogenous opioids. The role of these interactions in analgesia, tolerance and dependence is reviewed. Opioids inhibit the release of substance P from high threshold primary afferents, depress the activity of dorsal horn neurons and increase activity in serotonergic and noradrenergic neurons projecting from brainstem to spinal regions. Chronic administration of opioids modifies the dynamics of classical transmitters and those of endogenous opioid peptides in the brain, spinal cord and the pituitary gland. However, the effects observed are very variable. Several neuropeptides (vasopressin, MIF, alpha-MSH, CCK and dynorphin) have been reported to modify acute and chronic effects of opioids. Tolerance and dependence seen after opiate administration may involve changes in the function of these peptides.
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PMID:Opioid-neurotransmitter interactions: significance in analgesia, tolerance and dependence. 615 40

Most neuropeptides are known to occur both in the central nervous system and in blood. This, as well as the occurrence of central nervous peptide effects after peripheral administration, show the importance of studying the relationships between the peptides in the two compartments. For many peptides, such as the enkephalins, TRH, somatostatin and MIF-1, poor penetration of the blood-brain barrier was shown. In other cases, including beta-endorphin and angiotensin, peptides are rapidly degraded during or just after their entry into brain or cerebrospinal fluid. Some peptides, such as insulin, delta-sleep-inducing peptide, and the lipotropin-derived peptides, enter the cerebrospinal fluid to a slight or moderate extent in the intact form. Many peptide hormones, such as insulin, calcitonin and angiotensin, act directly on receptors in the circumventricular organs, where the blood-brain barrier is absent. Oxytocin, vasopressin, MSH, and an MSH-analog alter the properties of the blood-brain barrier, which may result in altered nutritient supply to the brain. In conclusion, the diffusion of most peptides across the brain vascular endothelium seems to be severely restricted. There are, however, several alternative routes for peripheral peptides to act on the central nervous system. The blood-brain barrier is a major obstacle for the development of pharmaceutically useful peptides, as in the case of synthetic enkephalin-analogs.
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PMID:Minireview. Peptides and the blood-brain barrier. 630 42

Rats maintained on 23-hr water deprivation were first trained to bar-press for continuous water reinforcement and then to discriminate between regularly alternating periods (24 sec) during which time a light signal was either on and each response was reinforced or the light was off and bar-presses were not rewarded. The following drugs were injected s. c. prior to the sessions of discriminative learning: piracetam, 1-(4-Methyl-piperazinocarbonylmethyl)-2-pyrrolidone/hydrogen maleate (VUFB 13763), N alpha-glycyl-glycyl[8-lysine]des-9-glycinamide-vasopressin (DG-Trigly-LVP) and an analog of MIF, EUC-Leu-beta-Ala-NH2 (EUC, 2-oxoimidazolidine-1-carboxylic acid). None of the drugs influenced the total number of bar-pressing (sum of reinforced and non reinforced responses). Piracetam (100 mg.kg-1), VUFB 13763 (40 mg.kg-1) and EUC-Leu-beta-Ala-NH2 (1 mg.kg-1) improved the performance of rats on the discrimination learning task, DG-Trigly-LVP slowed the rate of acquisition.
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PMID:Bar-pressing for water reward: effects of nootropic drugs and peptides on discrimination learning in rats. 647 74

Antidromically identified paraventricular neurones were recorded simultaneously with intramammary pressure in urethane (1.2 g/kg) anaesthetized rats during suckling. The correlation of the firing pattern of these neurones with milk ejection enabled distinction between oxytocin and vasopressin neurones. Oxytocin neurones displayed a short (2-6 s) characteristic high-frequency burst of spikes. This activation probably occurred simultaneously in all oxytocin neurones 12-18 s before milk ejection and was regular in both frequency and amplitude (total number of spikes). The role of neurohypophysial peptides and analogues in the control of these characteristics was studied. Injecting 10 pg, 100 pg and 1 ng of oxytocin into the 3rd ventricle increased background activity of slow-firing oxytocin neurones (less than 3 spikes/s) and had a strong dose-dependent facilitatory effect on the milk ejection reflex, increasing both the amplitude and frequency of neurosecretory bursts. No effect was observed on non-neurosecretory neurones. Such injection also triggered the milk ejection reflex when it had not appeared an hour after suckling began. Oxytocin did not itself induce neurosecretory activation, which only appeared if the young rats were sucking. Injecting oxytocin into the lateral ventricle was less effective than into the 3rd ventricle. No effect was observed after injection into the venous blood or into the 4th ventricle, which suggested that oxytocin acts in the hypothalamus. Injecting mesotocin or isotocin into the 3rd ventricle had a facilitatory effect similar to that of oxytocin but vasopressin, vasotocin, MIF I (pro-leu-gly-NH2, terminal triplet oxytocin) or bovine neurophysins I and II did not modify neurosecretory activation or the milk ejection pattern. Injecting an oxytocin antagonist, ([1(beta-mercapto-beta, beta cyclopentamethylene propionic acid), 8-ornithine] vasotocin, d(CH2)5OVT) into the 3rd ventricle decreased milk ejection frequency and considerably delayed the reappearance of the first milk ejection. This resulted from a decrease in both frequency and amplitude of neurosecretory bursts, which were too small to induce detectable oxytocin release. Moreover, d(CH2)5OVT suppressed the facilitatory effect of exogenous oxytocin. Under normal conditions, endogenous oxytocin seemed to be involved in the control of neurosecretory activation. Injecting 1 ng oxytocin or 1 or 10 ng vasopressin into the 3rd ventricle did not modify the firing pattern of vasopressin neurones whether activated by hyperosmotic stimulation (1 ml NaCl, 9% solution (w/v) I.P.) or not.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Electrophysiological evidence for facilitatory control of oxytocin neurones by oxytocin during suckling in the rat. 674 98


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