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 pimozide, a dopamine-receptor blocker and oxytocin, a neurohypophyseal neuropeptide were investigated in mice on the cocaine-induced exploratory hyperactivity. The action of oxytocin on changes of dopaminergic neurotransmission induced by cocaine was also measured. Cocaine-induced exploratory hyperactivity could be blocked by pimozide (1 mg kg-1, s.c.). Oxytocin (0.05-1.0 micrograms) inhibited the cocaine-induced hyperactivity in an U-shaped dose-response manner. In the nucleus accumbens, oxytocin antagonized the increased dopamine disappearance, elicited by cocaine, but not in the nucleus caudatus. The data suggest that oxytocin may influence the behavioural effect of cocaine by modulating dopaminergic neurotransmission in mesolimbic dopaminergic terminal region of the brain.
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PMID:Oxytocin attenuates the cocaine-induced exploratory hyperactivity in mice. 198 56

Frequency-responses curves for nerve stimulation and dose-response curve for norepinephrine, 5-hydroxytryptamine potassium chloride, vasopressin and acetylcholine (ACh) were determined in isolated, perfused mesenteric vascular beds from young (approximately 5 weeks) spontanelouly hypertensive (SHR) and Wistar Kyoto rats. Although mean systolic blood pressure (measured by tail cuff plethysmography) was slightly higher in the SHR, this difference was not significant. Slopes and maximum responses were increased significantly for nerve stimulation and all agonists. The basal perfusion pressure was also significantly elevated in the SHR. These differences are consistent with existing evidence that structural changes occur in blood vessels of SHR at an early stage and probably precede development of hypertension. Such structural changes could therefore contribute to development of the hypertension. Cocaine (1 microM) markedly increased responses to nerve stimulation and bolus injections of norepinephrine in preparations from SHR with little or no effect on such responses in Wistar Kyoto preparations, a result consistent with the known greater density of noradrenergic nerves in SHR vasculature. In the presence of cocaine, there was unmasked a selective super-sensitivity (significantly lower ED50) to norepinephrine in the SHR. Thus SHR mesenteric vessels may possess an alteration in adrenoreceptors or their coupling to other cellular mechanisms. Responses to ACh revealed no indication of a deficient endothelial mediated relaxation. An altered media:lumen ratio of small arteries, hypernoradrenergic innervation and supersensitivity to the transmitter may contribute to development of hypertension.
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PMID:Mesenteric vascular responses of young spontaneously hypertensive rats. 207 89

Cocaine is a widely used drug of abuse. One of the characteristic effects of this stimulant drug in the CNS of mice is the induction of motor hyperactivity. It was demonstrated that cocaine-induced motor hyperactivity could be blocked by pimozide, a dopamine receptor blocker, suggesting that dopamine was involved in cocaine-induced hyperactivity. Oxytocin, a neurohypophyseal neuropeptide, also partially antagonized cocaine-induced motor hyperactivity. Moreover, oxytocin antagonized the increased utilization of dopamine, elicited by cocaine in the nucleus accumbens. The data suggest that oxytocin may influence the behavioural effects of cocaine by affecting dopaminergic neurotransmission in some regions of the brain.
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PMID:The role of oxytocin-dopamine interactions in cocaine-induced locomotor hyperactivity. 216 Jun 23

The endocrine and neurochemical actions of cocaine in human and animal studies are reviewed. In humans, cocaine has been shown to influence plasma prolactin and growth hormone, as well as the dexamethasone suppression of cortisol and the thyroid-stimulating hormone response to thyroid-releasing hormone. In rats, cocaine affects plasma prolactin, luteinizing hormone, and testosterone, and can lead to adrenocortical hypertrophy. Behavioral sensitization to cocaine in rats has been shown to be related to the gender of the animals and appears to be modulated by vasopressin. A review of the neurochemical actions of cocaine indicates the important role of dopamine systems in the euphoric effects of the drug, as well as its withdrawal symptoms. Cocaine is a potent dopamine uptake inhibitor, as shown by its competition with [3H]GBR-12935 (a specific ligand for the dopamine uptake sites) for striatum binding sites. However, it does not acutely affect the high-affinity agonist sites of the D-2 dopamine receptors, which are suggested to be the active form of the presynaptic receptor. Using microdialysis techniques, cocaine is shown to rapidly cause a large increase of rat striatal dopamine levels, while its metabolites dihydroxyphenylacetic acid and homovanillic acid are slightly decreased and increased, respectively.
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PMID:Endocrine and neurochemical actions of cocaine. 268 66

1. The effects of cocaine and desipramine (DMI) on neuronal uptake (uptake1) of [3H]-noradrenaline (NA) and isometric tension development to exogenous NA were assessed in mesenteric resistance arteries of Wistar rats. 2. Both drugs concentration-dependently inhibited [3H]-NA uptake1, DMI being more potent than cocaine. The maximum inhibition produced by each drug was the same as that produced by denervation with 6-hydroxydopamine. In denervated vessels there was no effect of cocaine on [3H]-NA uptake1. 3. Cocaine, in the same concentration range which caused inhibition of uptake1, increased the sensitivity to NA, while DMI, in a concentration range which inhibited uptake1, did not increase the sensitivity to NA and at high concentrations reduced the sensitivity and maximal response to NA. Since DMI affected responses to NA but not responses to vasopressin and potassium its effect is probably related to blockade of alpha 1-adrenoceptors. 4. We conclude that the effect of cocaine on the sensitivity to NA reflects inhibition of uptake1 in rat resistance arteries, while DMI cannot be used to assess the functional effect of uptake1 in this preparation.
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PMID:The effect of cocaine and desipramine on neuronal uptake of [3H]-noradrenaline and sensitivity to noradrenaline of rat mesenteric resistance arteries. 781 21

Neuroendocrine pharmacology represents a potentially valuable approach to the assessment of alterations in neuronal function in the brain of human cocaine abusers. Neuroendocrine effects of the monoamine uptake inhibitor cocaine have predominantly been examined in laboratory animals. These preclinical studies may help to identify the optimal challenge tests to be performed in clinical studies. In laboratory animals, acute administration of cocaine activates the hypothalamic-pituitary-adrenal axis, via actions on serotonergic and dopaminergic neurons in the brain. Cocaine also reduces prolactin secretion, probably by dopaminergic mechanisms, although the necessary studies to confirm this hypothesis have not been performed. Cocaine also reduces renin secretion, and increases vasopressin and luteinizing hormone secretion, by mechanisms which have not been clearly established. The adrenocorticotropin, corticosterone, prolactin, and renin responses to cocaine are generally unaltered by prior cocaine exposure, suggesting that tolerance or sensitization to the endocrine effects of cocaine does not occur. However, several studies have determined that prior cocaine exposure alters the serotonergic regulation of hormone secretion. Chronic cocaine exposure reduces some of the hormone responses to the serotonin (5-HT) releasers p-chloroamphetamine and d-fenfluramine, suggesting deficits in the functional status of serotonergic nerve terminals. Additionally, repeated cocaine exposure produces subsensitive 5-HT1A-mediated hormone responses, and supersensitive 5-HT2-mediated responses. Alterations in dopaminergic- or noradrenergic-mediated hormone responses have not been examined in animals chronically exposed to cocaine. Endocrine studies in human cocaine abusers have largely examined basal hormone levels or the hormone responses to cocaine. Strong conclusions from these studies are limited because (1) many neuronal and nonneuronal systems regulate secretion of each hormone, so that alterations in basal hormone levels cannot be attributed to only one neurotransmitter; and (2) hormone responses to cocaine cannot be examined in cocaine-naive subjects due to ethical considerations, making it impossible to determine whether the response in cocaine abusers is abnormal. It may be more beneficial for studies in cocaine abusers to examine the hormone responses to drugs that specifically affect monoaminergic neurons and compare the data with cocaine-naive individuals.
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PMID:Monoaminergic regulation of neuroendocrine function and its modification by cocaine. 781 44

The effects of arginine8-vasopressin on the stimulation of locomotor activity induced by ethanol, cocaine and amphetamine were examined in DBA/2N mice. Locomotor activity was measured by photocell beam interruption for a period of 45 min following ethanol, cocaine or amphetamine administration. Pretreatment with vasopressin alone in a dose of 2 (but not 1) microg/mouse s.c. reduced locomotor activity. The low dose of vasopressin did not modify the stimulation of locomotor activity induced by i.p. administration of ethanol in doses of either 1.5 or 2 g/kg. The high dose of vasopressin reduced locomotor activity induced by both doses of ethanol, in an apparently additive manner. Cocaine in doses of 15 and 20 mg/kg strongly stimulated locomotor activity, but this stimulation was completely antagonized by pretreatment with 1 microg of vasopressin. Similarly, the stimulation of locomotor activity induced by amphetamine (5 mg/kg) was also blocked by pretreatment with vasopressin. These findings raise the possibility that the effect of vasopressin varies with the extent and nature of dopaminergic involvement in the drug-induced stimulation of activity. For drugs like cocaine or amphetamine which stimulate locomotor activity primarily through the mesolimbic dopaminergic system, vasopressin can completely antagonize the stimulation. For ethanol, which stimulates locomotor activity through action on a number of other neurotransmitters as well as dopamine, vasopressin treatment only reduces its stimulation of locomotor activity in an additive manner. These results suggest a close interaction between vasopressin and dopamine action.
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PMID:Vasopressin opposes locomotor stimulation by ethanol, cocaine and amphetamine in mice. 975 33

Cocaine and amphetamine regulated transcript (CART) has been identified as one of the most abundant mRNAs in the rat hypothalamus. The objective of the present study was to elucidate the distribution of CART peptide immunoreactive (CARTir) neurons in the monkey hypothalamus and characterize their ultrastructural features and synaptic connections in the paraventricular nucleus (PVN). CARTir neurons were particularly abundant in the PVN, supraoptic nucleus (SON), infundibular nucleus, and premammillary nucleus, whereas the anterior, lateral, and posterior hypothalamic areas as well as the posterior nucleus displayed moderate immunoreactivity. Dense bundles of CARTir fibers exited the PVN and SON and followed a trajectory to the infundibulum similar to that previously shown for vasopressin and oxytocin fibers. The posterior pituitary was densely packed with large CARTir varicosities which, in some cases, were apposed to labeled pituicytes. The external/palisade zone of the median eminence contained rich plexuses of small CARTir varicose fibers, and the internal/fibrous zone was enriched in large axon-like processes. Electron microscope analysis of the PVN revealed (1) that CART peptide immunoreactivity is found in neurosecretory and non-neurosecretory neurons contacted predominantly by unlabelled terminals forming asymmetric synapses, (2) that CARTir terminals resemble glutamatergic and/or noradrenergic boutons and form asymmetric synapses with non-neurosecretory dendrites, and (3) that neuropeptide Y (NPY)-containing terminals are apposed to CARTir neurons in the medial part of the nucleus. In conclusion, our findings demonstrate that CART peptide is abundant in neuronal perikarya and axon terminals throughout the monkey hypothalamus and along the hypothalamopituitary axis. This strengthens the idea that CART peptides may act as putative neurotansmitters/neuromodulators that mediate various neuroendocrine and autonomic functions in primates.
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PMID:CART peptide immunoreactivity in the hypothalamus and pituitary in monkeys: analysis of ultrastructural features and synaptic connections in the paraventricular nucleus. 1060 89

CD81, a tetraspanin transmembrane protein involved in cell adhesion, was found by differential display to be upregulated in the nucleus accumbens of rat brain following acute cocaine treatment (four injections of 30 mg/kg every 2 h followed by 24 h withdrawal). Cocaine-induced expression of CD81 in adult rat brain was confirmed by quantitative real-time RT-PCR. Its expression in neurons and its function in the brain are unknown. In situ hybridization shows a neuron-specific expression pattern in brain regions functionally related to the regulation of cardiovascular function and fluid homeostasis. CD81 displays codistribution to galanin and, to a lesser extent, to vasopressin. These findings add to data that suggest a connection between the brain reward pathway and the centers regulating endocrine and autonomic functions, in relation to neurochemical, behavioral, and somatic consequences of drug abuse.
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PMID:Cocaine-induced expression of the tetraspanin CD81 and its relation to hypothalamic function. 1117 68

Although uncommon, medication-induced colonotoxicity is important to recognize because medication cessation generally leads to prompt clinical improvement, while medication continuation results in disease exacerbation. This review categorizes the association between medications and colonotoxicity as "well-established" or "probable," according to the following criteria: total number of reported cases, number of different research groups reporting an association, experimental and pharmacologic evidence of an association, and validity of an association in each reported case. Cocaine, ergotamine, estrogen, sodium polystyrene, alosetron, amphetamines, pseudoephedrine, and vasopressin are associated with colonic ischemia. The mechanisms include vasospasm, thrombogenesis, and shunting of blood from mesenteric vessels. Narcotics, phenothiazines, vincristine, atropine, nifedipine, and tricyclic antidepressants are associated with colonic pseudo-obstruction. The mechanisms include antagonizing prokinetic neurotransmitters, stimulating antikinetic neurotransmitters, promoting dysmotility, relaxing smooth muscle, and injuring enteric neurons. Numerous antibiotics are associated with pseudomembranous colitis; ampicillin is associated with hemorrhagic colitis; chemotherapy is associated with neutropenic colitis; and deferoxamine is associated with Yersinia enterocolitis. Mechanisms of these toxicities include altering normal bowel flora, weakening immunologic defenses, promoting microorganism virulence, and mucosal injury. Gold compounds, nonsteroidal antiinflammatory drugs, alpha-methyldopa, salicylates, and sulfasalazine are associated with an inflammatory or cytotoxic colitis. The mechanisms include direct mucosal cytotoxicity, antimetabolite effects, or drug allergy. Nonsteroidal antiinflammatory drugs, cyclo 3 fort, flutamide, lansoprazole, and ticlopidine are associated with lymphocytic colitis. The mechanisms include immunologic activation or attenuated immunologic defenses. Chronic cathartic use leads to colonic hypomotility and abdominal distention. Intrarectally administered corrosive compounds can produce a toxic colitis.
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PMID:Colonic toxicity of administered drugs and chemicals. 1518 Jul 42


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