Elsevier

Peptides

Volume 5, Issue 4, July–August 1984, Pages 747-756
Peptides

Vasopressin analgesia: Specificity of action and non-opioid effects

https://doi.org/10.1016/0196-9781(84)90017-2Get rights and content

Abstract

Recent neuroanatomical and behavioral evidence has indicated that vasopressin (VP) increases pain thresholds. In the present study intracerebroventricular (ICV) administration of both arginine VP (AVP: 75–500 ng) and 1-deamino-8-D-arginine vasopressin (DDAVP: 150–500 ng) elevated tail flick latencies. Oxytocin (OXY, ICV), also elevated tail-flick latencies (150–1000 ng); however this increase was accompanied by “barrel-roll” seizure activity. VP analgesia was eliminated by pretreatment with 1-deamino-penicillamine-2(O-methyl)tyrosine-AVP (dPTyr(me)AVP: 500 ng, ICV), a VP antagonist, but not naloxone (1 or 10 μg, ICV), suggesting that VP modulates nonciceptive thresholds through its own binding sites. Conversely, pretreatment with naloxone (1 μg, ICV) but not dPTyr(me)AVP (1μg, ICV) attenuated the analgesic efficacy of systemic morphine (10 mg/kg), further dissociating VP and central opiate analgesic processes. Finally, systemic pretreatment with dexamethasone potentiated VP analgesia. These data support the notion that VP is a specific non-opioid pain inhibitor.

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    Present address: Department of Anatomy, Box 603, University of Rochester School of Medicine, 601 Elmwood Ave., Rochester, NY 14642.

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