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

Endogenous arginine vasopressin was previously shown to modulate the rate of loss of functional (CNS) tolerance to ethanol, suggesting that chronic ethanol ingestion might alter vasopressin synthesis and/or release. Since extrahypothalamic vasopressin is believed to be involved in the CNS effects of the peptide, we determined the effect of ethanol on vasopressin mRNA in the bed nucleus of the stria terminalis (BST), as well as in several hypothalamic nuclei. Chronic ethanol ingestion, that produced functional tolerance and physical dependence in mice, resulted in decreased vasopressin mRNA levels in all areas examined. In contrast, as expected, dehydration resulted in increases in vasopressin mRNA in the BST and in all hypothalamic nuclei except the suprachiasmatic nucleus. In the BST, both ethanol ingestion and dehydration affected cells in the central region of the nucleus, while cells in the caudal portion were only affected by ethanol treatment. The results indicate that chronic ethanol ingestion generally reduces the synthesis of vasopressin, and that increased vasopressin synthesis is not necessary in order for the peptide to affect ethanol tolerance.
 ...
PMID:Chronic ethanol ingestion decreases vasopressin mRNA in hypothalamic and extrahypothalamic nuclei of mouse brain. 174 46

The recent investigations on biochemical and biophysical mechanisms of ethanol in acute intoxication, tolerance and physical dependence suggest that the cell membrane, intracellular metabolism and central neurotransmitters are involved. In acute intoxication ethanol increases the "fluidity" of the cell membrane and stimulates the central gabergic system. In alcoholics, the body adapts, and in the presence of ethanol, the cell membrane becomes more "rigid" and the gabergic system hypoactive. When alcohol intake is discontinued the hypoactivity of the gabergic system is unmasked and it is manifested as withdrawal syndrome. The alcohol intake compensates for the clinical symptoms of decreased gabergic activity and thereby continuously prevent the onset of withdrawal symptoms. On the other hand, intact central noradrenergic and 5-hydroxytryptaminergic systems as well as the neuropeptide vasopressin maintain the tolerance. After withdrawal syndrome, membrane alterations and the state of diminished gabergic activity gradually return to normal. This period of slow recuperation corresponds to the subacute withdrawal syndrome. In this period, there is a continuous desire for alcohol intake. Further, alcoholics, in this situation, are very vulnerable with feelings of insecurity, fragility and isolation. All these factors additionally induce a latent desire for ethanol. It follows then that a stimulation of decreased gabergic activity is a new approach in drug therapy of alcoholism. One of these new stimulants is acamprosate. The new substance is a structural analogue of GABA and acts as an agonist on gabergic receptors. Therefore, acamprosate improves the central gabergic activity. Alcoholics treated with acamprosate stated that they no longer felt a desire for alcohol intake. In this way, acamprosate maintains the abstinence for several months during the post-withdrawal phase.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Modern drug therapy in alcoholism]. 180 68

The effect of oxytocin (OXT) and vasopressin (VP) on alcohol withdrawal was investigated. CFLP mice were treated with alternating daily injections of tert-butanol and ethanol for four days, which resulted in physical dependence on ethanol. The severity of withdrawal symptoms was assessed by picrotoxin. The lowest dose (0.02 IU) of each of the peptides precipitated tonic convulsions, while higher doses resulted in different tendencies. OXT-treated mice displayed milder withdrawal symptoms in response to increasing doses of peptide (0.2-2.0 IU). VP showed a U-shaped dose-response effect. The lowest (0.02 IU) and the highest (2.0 IU) doses increased the occurrence of withdrawal convulsions and the frequency of deaths.
 ...
PMID:Effects of neurohypophyseal peptide hormones on alcohol dependence and withdrawal. 359 87

Among the many factors that may influence the development or expression of functional tolerance to or physical dependence on ethanol is the neurohypophyseal hormone, arginine vasopressin (AVP). This peptide hormone, administered exogenously, maintains ethanol tolerance in animals once such tolerance has been established. An analog of the hormone has also been reported to facilitate the development of ethanol tolerance and to exacerbate ethanol withdrawal symptomatology. Neurohypophyseal hormones and structurally related peptides have previously been shown to influence learning or memory; however, structure-activity analyses reveal differences in the structural requirements for maintenance of ethanol tolerance as compared to facilitation of memory processes. Therefore, these phenomena may represent CNS adaptive processes which are subserved by different mechanisms, or are differentially sensitive to particular peptides. The initial sensitivity of an animal to ethanol can also be affected by peptides, notably thyrotropin releasing hormone (thyroliberin, TRH). TRH antagonizes many of the initial responses to ethanol, perhaps by non-specific means. AVP, however, appears to potentiate the sedative effect of an acute dose of ethanol. Neurohypophyseal peptides also modulate ethanol intake. Thus, these neuropeptides, which have been localized to many areas of brain, may serve as endogenous modulators of various parameters related to ethanol consumption.
 ...
PMID:Centrally acting peptides and tolerance to ethanol. 612 10

Evidence exists to suggest that there are neurochemical responses common to the development of tolerance to and dependence on a variety of psychoactive drugs. Experimental data indicates that pituitary peptides such as corticotropin and vasopressin, in addition to the endorphins, influence the development of physical dependence on either morphine or ethanol. If these findings are supported by further investigations with human subjects, various manipulations of pituitary-adrenal function, such as the administration of corticotropin and vasopressin analogs or drugs such as dexamethasone, may prove to be of clinical utility.
 ...
PMID:Neuropeptide modulation of opiate and ethanol tolerance and dependence. 625 14

Mice were rendered physically dependent on ethanol by inhalation of ethanol vapour and treatment with pyrazole for 3 days. On Day 4, withdrawal convulsions were measured and on Day 5 or later, residual tolerance to the hypothermic effect of an i.p. challenge dose of 3 g/kg ethanol was assessed. Mice continuously infused with the vasopressin fragment des-Gly9-[Arg8]-vasopressin dicitrate (DGAVP) throughout the periods of dependence induction and withdrawal testing exhibited exacerbated withdrawal convulsions. DGAVP also tended to exacerbate withdrawal when injected s.c. repeatedly (10 micrograms/injection/mouse) during testing for withdrawal. The data indicate that these effects were not likely to have been due to subconvulsive activity of DGAVP by itself or to changes in blood levels of ethanol. Continuous infusion of DGAVP enhanced residual tolerance on Day 5 but did not maintain tolerance when the time interval between withdrawal and testing for tolerance was increased. Restricting treatment with DGAVP to the period of induction of dependence (Days 1-3) also enhanced tolerance on Day 5. The data indicate that the vasopressin fragment modulates the development and/or the decay of tolerance to ethanol. In addition it exacerbates withdrawal convulsions, an effect that may be due to modulation of physical dependence.
 ...
PMID:Tolerance to ethanol and severity of withdrawal in mice are enhanced by a vasopressin fragment. 719 31