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.
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||1 36-1|
|Publication status||Published - Jan 1 1994|
All Science Journal Classification (ASJC) codes
- Physiology (medical)