EP(1)-RECEPTOR MEDIATION OF PROSTAGLANDIN E(2)-INDUCED HYPERTHERMIA IN RATS

被引:50
|
作者
OKA, T
HORI, T
机构
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1994年 / 267卷 / 01期
关键词
PROSTAGLANDIN E(2); FEVER; EP(1) RECEPTOR; 17-PHENYL-OMEGA-TRINORPROSTAGLANDIN; E(2); SC-19220;
D O I
10.1152/ajpregu.1994.267.1.R289
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
To investigate what type of prostanoid receptors are involved in the development of fever induced by brain prostaglandin E(2) (PGE(2)), PGE(2) 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 degrees C environment. 17-Phenyl-omega-trinor-PGE(2) (an EP(1) agonist; 0.01-10 nmol) produced a rapid and dose-dependent rise in T-co. Even though the EP(1) agonist was 10 times less potent than PGE(2) on a molar basis, the time course of this hyperthermia was quite similar to that of the PGE(2)-induced one. No fever was elicited by an LCV injection of butaprost (an EP(2) agonist; 0.1-100 nmol), 11-deoxy-PGE(1) (an EP(2) agonist; 0.1-1.0 nmol), or MB-28767 (an EP(3) agonist; 0.01-1.0 nmol). The PGE(2) (0.3 nmol)-induced hyperthermia was blocked by LCV pretreatment with SC-19220 (150 nmol), an EP(1) antagonist. The results suggest that the PGE(2)-induced hyperthermia in the rat is mediated predominantly through EP(1) receptors in the brain.
引用
收藏
页码:R289 / R294
页数:6
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