EP1-receptor mediation of prostaglandin E2-induced hyperthermia in rats

T. Oka, T. Hori

研究成果: Contribution to journalArticle査読

52 被引用数 (Scopus)

抄録

To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E2 (PGE2), PGE2 and its analogues were injected into a lateral cerebroventricle (LCV) of rats, and the changes in colonic temperature (T(co)) were observed in a 23 ± 1°C environment. 17-Phenyl-ω-trinor-PGE2 (an EP1 agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in T(co). Even though the EP1 agonist was 10 times less potent than PGE2 on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE2-induced one. No fever was elicited by an LCV injection of butaprost (an EP2 agonist; 0.1- 100 nmol), 11-deoxy-PGE1 (an EP2 agonist; 0.1-1.0 nmol), or MB-28767 (an EP3 agonist; 0.01-1.0 nmol). The PGE2 (0.3 nmol)-induced hyperthermia was blocked by LCV pretreatment with SC-19220 (150 nmol), an EP1 antagonist. The results suggest that the PGE2-induced hyperthermia in the rat is mediated predominantly through EP1 receptors in the brain.

本文言語英語
ページ(範囲)R289-R294
ジャーナルAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
267
1 36-1
DOI
出版ステータス出版済み - 1994

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

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