Urinary cyclic AMP and vasopressin excretion in rat strains selected for their alcohol intake

Linkola, Jaakko; Fyhrquist, Frej

doi:10.1111/j.1748-1716.1978.tb06083.x

Cited by 7 publications

(1 citation statement)

References 14 publications

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“…When comparing alcoholics to more alcohol naïve individuals, alcoholics were found to have a more pronounced decrease in plasma VP levels when drinking (Collins et al 1992; Hirschl et al 1994), suppressed VP levels even during alcohol withdrawal (Doring et al 2003; Hirschl et al 1994; Jahn et al 2004; Trabert et al 1992), and a lack of a VP increase in response to novelty (Ehrenreich et al 1997). Similarly, differences in urine VP (urine VP being an approximate measure of plasma VP) are found between alcohol preferring (AA rats) and alcohol non-preferring rats (ANA) (Linkola and Fyhrquist 1978; Linkola et al 1977). However the two studies do not agree on the directionality of the difference as one study found a decrease in urine VP in AA rats compared to ANA rats and the other an increase in urine VP in AA rats compared to ANA rats.…”

Section: Alcohol’s Effect On the Vp Systemmentioning

confidence: 97%

Vasopressin and alcohol: a multifaceted relationship

et al. 2018

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Background: Arginine vasopressin (VP) has been implicated in a number of neuropsychiatric disorders with an emphasis on situations were stress increased the severity of the disorder. Based on this hypothesized role for VP in neuropsychiatric disorders, much research is currently being undertaken in humans and animals to test VP as a target for treatment of a number of these disorders including alcohol abuse. Objectives: To provide a summary of the literature regarding the role of VP in alcohol and stress related behaviors including the use of drugs that target VP in clinical trials. Results: Changes in various components of the VP system occur with alcohol and stress. Manipulating VP or its receptors can alter alcohol and stress related behaviors including tolerance to alcohol, alcohol drinking, and anxiety-like behavior. Finally, the HPA axis response to alcohol is also altered by manipulating the VP system. However, clinical trials of VP antagonists have had mixed results. Conclusions: A review of VP’s involvement in alcohol’s actions demonstrates that there is much to be learned about brain regions involved in VP-mediated effects on behavior. Thus, future work should focus on elucidating relevant brain regions. By using previous knowledge of the actions of VP and determining the brain regions and/or systems involved in its different behavioral effects, it may be possible to identify a specific receptor subtype target, drug treatment combination, or specific clinical contexts that may point toward a more successful treatment.

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