Activation of ACTH release is mediated by the same molecule as the final mediator, PGE2, of febrile response in rats.
Increase in the blood level of adrenocorticotropic hormone (ACTH) and fever are induced by i.v. administration of interleukin-1 alpha (IL-1 alpha) in rats. With preinjection of indomethacin, the ACTH and fever responses to i.v. IL-1 alpha were both either greatly reduced or abolished. Intrapreoptic microinjection of prostaglandin E2 (PGE2) caused ACTH and fever responses similar to those seen after i.v. IL-1 alpha. These data suggest that PGE2, a final mediator of fever, may be released by i.v. IL-1 alpha and also act centrally to enhance the release of corticotropic-releasing factor in the brain.
Murakami
N
N
Department of Physiology, Yamaguchi University School of Medicine, Japan.
Watanabe
T
T
D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D003346:Corticotropin-Releasing Hormone / Q000378:metabolism; D015232:Dinoprostone / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D005334:Fever / Q000139:chemically induced* / Q000378:metabolism; D007213:Indomethacin / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology*; D008297:Male; D011301:Preoptic Area / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology; D051381:Rats; D011919:Rats, Inbred Strains
D007375:Interleukin-1; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D015232:Dinoprostone; D007213:Indomethacin