Vasopressin analgesia: Specificity of action and non-opioid effects

Jeffrey H. Kordower, Richard J. Bodnar

Research output: Contribution to journalArticlepeer-review

64 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)747-756
Number of pages10
JournalPeptides
Volume5
Issue number4
DOIs
StatePublished - 1984
Externally publishedYes

Keywords

  • 1-deamino-8-D-arginine vasopressin
  • Arginine vasopressin
  • Oxytocin
  • Pain
  • dPTyr(me)AVP

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Endocrinology
  • Cellular and Molecular Neuroscience

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