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Journal of Neuroscience, Vol 14, 1985-1993, Copyright © 1994 by Society for Neuroscience
In the rat, endogenous nitric oxide modulates the response of the hypothalamic-pituitary-adrenal axis to interleukin-1 beta, vasopressin, and oxytocin
C Rivier and GH Shen
Clayton Foundation Laboratories for Peptide Biology, Salk Institute, La Jolla, California 92037.
Nitric oxide (NO) synthase (NOS), the enzyme responsible for NO formation,
is found in hypothalamic neurons containing oxytocin (OT), vasopressin
(VP), and to a lesser extent corticotropin-releasing factor (CRF). Because
NO is reported to modulate endocrine activity, we have investigated the
hypothesis that endogenous NO participates in ACTH released by various
secretagogues in the rat. In the adult male rat, the intravenous injection
of interleukin-1 beta (IL-1 beta; 0.2-0.3 micrograms/kg), VP (0.3-0.9
micrograms/kg), and OT (30 micrograms/kg) significantly increased plasma
ACTH and corticosterone levels. Pretreatment with the L-form, but not the
D-form, of N omega nitro-L- arginine-methylester (L-NAME; a specific
inhibitor of NOS) markedly augmented the effects of these secretagogues
whether it was injected acutely or over a 4 d period. Blockade of NOS
activity also caused significant (P < 0.01) extensions of the duration
of action of IL-1 beta, VP, and OT. In contrast, L-NAME did not
significantly alter the stimulatory action of peripherally injected CRF, or
centrally administered IL-1 beta. Administration of L-arginine, but not D-
arginine (100 mg/kg), used as a substrate for basal NO synthesis and which
did not by itself alter the activity of the hypothalamic- pituitary-adrenal
(HPA) axis, blunted IL-1-induced ACTH secretion, and reversed the
interaction between L-NAME and IL-1 beta. The stimulatory action of
endotoxin, a lipopolysaccharide that releases endogenous cytokines, was
also augmented by inhibition of NO formation.(ABSTRACT TRUNCATED AT 250
WORDS)
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