Involvement of EP3 subtype of prostaglandin E receptors in PGE2-induced enhancement of the bradykinin response of nociceptors

Brain Res. 1993 Dec 31;632(1-2):321-4. doi: 10.1016/0006-8993(93)91169-s.

Abstract

Prostaglandin E2 augments bradykinin-induced discharges of polymodal receptors as studied in vitro preparations. The antagonist and agonists for three subtypes of EP receptors were used to determine which subtype is involved in this phenomenon. The agonist for EP3 (M&B28767) simulated the PGE2-induced effect but not for EP2 (butaprost). The antagonist for EP1 (AH6809) did not suppress the effect. These findings indicate the involvement of the EP3 receptor subtype in the effect.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alprostadil / analogs & derivatives
  • Alprostadil / pharmacology
  • Animals
  • Bradykinin / pharmacology*
  • Dinoprostone / pharmacology*
  • Dogs
  • Dose-Response Relationship, Drug
  • Drug Synergism
  • Epididymis / physiology
  • Hot Temperature
  • In Vitro Techniques
  • Male
  • Nociceptors / drug effects
  • Nociceptors / physiology*
  • Physical Stimulation
  • Prostaglandin Antagonists / pharmacology
  • Receptors, Prostaglandin E / drug effects
  • Receptors, Prostaglandin E / physiology*
  • Testis / physiology
  • Xanthenes / pharmacology
  • Xanthones*

Substances

  • Prostaglandin Antagonists
  • Receptors, Prostaglandin E
  • Xanthenes
  • Xanthones
  • 6-isopropoxy-9-oxoxanthene-2-carboxylic acid
  • 11-deoxy-16-phenoxy-17,18,19,20-tetranorprostaglandin E1
  • Alprostadil
  • butaprost
  • Dinoprostone
  • Bradykinin