RT Journal Article
SR Electronic
T1 Glucocorticoid Enhances Interleukin-1-Induced Pressor Response in Freely Moving Rats Through Its Effect on Nitric Oxide Release
JF Journal of Pharmacology and Experimental Therapeutics
JO J Pharmacol Exp Ther
FD American Society for Pharmacology and Experimental Therapeutics
SP 24
OP 30
VO 289
IS 1
A1 Tatsuo Watanabe
A1 Yoshiyuki Sakata
A1 Takashi Fujioka
A1 Daikai Sadamitsu
A1 Tsuyoshi Maekawa
YR 1999
UL http://jpet.aspetjournals.org/content/289/1/24.abstract
AB We investigated whether changes in nitric oxide (NO) release might be responsible for the modulation by glucocorticoids of the pressor response to i.p. injection of interleukin-1β (IL-1β) in freely moving rats. In such rats, IL-1β (10 μg/kg) induced a biphasic pressor response, with a rise in the plasma concentration of NOx (NO2− andNO3− : metabolites of NO) during the second phase. Systemic pretreatment with an exogenous glucocorticoid, dexamethasone (0.5 mg/kg), enhanced the second phase of the pressor response and completely suppressed the increase in plasma NOx. Treatment withNω-nitro-l-arginine methyl ester (l-NAME, a nonspecific NO synthase inhibitor), enhanced the pressor response while attenuating the increase in plasma NOx. After bilateral adrenalectomy, IL-1β induced a smaller pressor response, but a larger increase in plasma NOx; dexamethasone reversed these changes. Our results suggest that endogenous NO moderates the pressor response to IL-1β in freely moving rats, and that glucocorticoids enhance the IL-1β-induced pressor response at least in part by reducing endogenous NO release. The American Society for Pharmacology and Experimental Therapeutics