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Comparison of prostaglandin E1- and prostaglandin E2-induced hyperalgesia in the rat

Publication Date
DOI: 10.1016/0306-4522(94)90369-7
  • Damgo
  • [D-Ala2
  • N-Me-Phe4
  • Gly5-Ol] Enkephalin
  • Dhla
  • Dihomo-γ-Linolenic Acid
  • Ep1–3Receptor
  • E-Type 1–3 Prostaglandin Receptor
  • GdpβS
  • Guanosine 5'-O-(2-Thiodiphosphate)
  • G-Protein
  • Guanine Nucleotide-Binding Regulatory Protein
  • Pge1
  • Prostaglandin E1
  • Pge2
  • Prostaglandin E2Pgi2
  • Prostacyclin
  • 8R
  • 15S-Dihete
  • 8R
  • 15S-Dihydoxyicosatetroenoic Acid
  • Sc19220
  • L-Acetyl-2-(8-Chloro-10
  • 11-Dihydrodibenz [B
  • F]
  • [1
  • 4]Oxazepine-10-Carbonyl ( )Hydrazine
  • Sc51089
  • 8-Chlorodibenz [B
  • F] [1
  • 4]Oxazepine-10(11
  • 4)-Carboxylic
  • Acid
  • Stz
  • Streptozotocin
  • Stz-D
  • Streptozotocin-Induced Diabetes
  • Biology


Abstract We have studied prostaglandin E 1-induced mechanical hyperalgesia in the rat hindpaw, by assessing paw-withdrawal thresholds, before and after injecting prostaglandin E 1 alone or with other agents, in normal and streptozotocin-induced diabetic rats. In normal and diabetic rats, prostaglandin E 1 (1–1000 ng) produced a dose-dependent decrease in mechanical nociceptive threshold. In diabetic rats, prostaglandin E 1 was more potent than in normal rats, in producing hyperalgesia, whereas prostaglandin E 2 hyperalgesia was not changed in normal and diabetic rats. Prostaglandin Ei-induced hyperalgesia was not inhibited by E-type 1 prostaglandin receptor antagonists, SC 19220 or SC51089, either in normal or diabetic rats. In fact, in the presence of SC19220, prostaglandin E 1 produced enhanced hyperalgesia, in normal rats. Prostaglandin E 1 hyperalgesia was not significantly modified by sympathectomy or indomethacin. Unlike prostaglandin E 2, prostaglandin E 1 hyperalgesia was not blocked by the inhibitor of the stimulatory guanine nucleotide-binding regulatory protein, guanosine 5'-O-(2-thiodiphosphate). It is suggested that prostaglandin E 1 decreases primary afferent nociceptive threshold directly, by activating a prostaglandin receptor other than the E-type 1 prostaglandin receptor, and that this receptor is not coupled to a stimulatory guanine nucleotide-binding regulatory protein.

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