Korean J Physiol Pharmacol.
2001 Feb;5(1):93-98.
The hyperthermic effect of nitric oxide in central nervous system
- Affiliations
-
- 1College of Pharmacy, Sungkyunkwan University, Suwon, South Korea.
sylee@skku.ac.kr
Abstract
- The precise mechanism of set-point regulation in hypothalamus was not
elucidated. Nitric oxide synthases (NOS) were detected in hypothalamus,
however, the roles of NO in hypothalamus was not fully studied. So, we
tested the effects of NO on body temperature because preoptic-anterior
hypothalamus was known as the presumptive primary fever-producing site.
NO donor sodium nitroprusside (SNP, 4 nmol, i.c.v.) elicited marked
febrile response, and this febrile response was completely blocked by
indomethacin (a cyclooxygenase inhibitor). But, ODQ (selective
guanylate cyclase inhibitor, 50 microgram, i.c.v.) did not inhibit fever
induced by SNP. The cyclic GMP analogue dibutyryl-cGMP (100 microgram,
i.c.v.) induced significant pyreses, which is blocked by indomethacin.
NG-nitro-L-arginine methyl ester (L-NAME, non selective NOS inhibitor)
inhibited fever induced by interleukin-1 beta (IL-1 beta, 10 ng,
i.c.v.), one of endogenous pyrogens. These results indicate that NO may
have an important role, not related to stimulation of soluble guanylate
cyclase, in the signal pathway of thermoregulation in hypothalamus.