Mechanisms of adrenaline-induced antinociception in mice

Chin J Physiol. 1992;35(3):205-10.

Abstract

Infusion of adrenaline into the upper lumbar subarachnoid space in lightly anesthetized mice produced a significant elevation of the nociceptive threshold as quantitated by tail flick test. The antinociceptive effect of adrenaline was dose-dependent and antagonized equally by pretreatment with either alpha-1 selective antagonist prazosin or alpha-2 selective antagonist yohimbine at a dose of 0.05 microgram/5 microliter/mouse. This antinociceptive effect of adrenaline was also blocked by pretreatment with beta antagonist propranolol or opiate antagonist naloxone at higher doses, i.e., 0.5 microgram and 1.0 microgram/5 microliter/mouse, respectively. These results suggest that the antinociceptive mechanisms of adrenaline at the lumbar spinal level in the mouse seem to be mediated not only through alpha- and beta-adrenergic pathways but also through opiate system.

MeSH terms

  • Analgesics / administration & dosage
  • Analgesics / pharmacology*
  • Animals
  • Epinephrine / administration & dosage
  • Epinephrine / pharmacology*
  • Injections, Spinal
  • Male
  • Mice
  • Mice, Inbred ICR
  • Naloxone / pharmacology
  • Pain / physiopathology
  • Pain / prevention & control*
  • Prazosin / pharmacology
  • Propranolol / pharmacology
  • Sensory Thresholds / drug effects
  • Yohimbine / pharmacology

Substances

  • Analgesics
  • Yohimbine
  • Naloxone
  • Propranolol
  • Prazosin
  • Epinephrine