title: Relative importance of nitric oxide and carbon monoxide in regulating the ACTH response to immune and non-immune signals.
abstract: The present work investigated the effect of nitric oxide (NO) or carbon monoxide (CO) in the ACTH response to an immune signal [the intravenous injection of interleukin-1 β (IL-1β)] or to a neurogenic stressor (mild intermittent inescapable foot shocks). The arginine derivative N(ω)-L-arginine methylester (L-NAME), which non-specifically inhibits NO formation induced by all constitutive forms of NO synthase (NOS), significantly augmented the effect of IL-1P,but blockade of CO formation with metalloporphyrins was without effect. On the other hand, L-NAME blunted the effect of shocks on the early phase of ACTH release, while we had reported earlier that metalloporphyrins exerted a similar effect. This effect was mimicked by blockade of neuronal (n) NOS by N(ω)-Propyl-L-arginine (PA), although the resulting decrease in hormone levels was less than that induced by L-NAME. These results indicate that endogenous NO, but not CO, interferes with ACTH released by a peripheral immune signal. In contrast, NO formed by nNOS enhances the ability of shocks to induce ACTH secretion.
authors.affiliation: The Clayton Foundation Laboratories for Peptide Siology, The Salk Institute, La Jolla, CA 92037, USA. crivier@salk.edu
authors.forename: C
authors.initials: C
authors.lastname: Rivier
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D002248:Carbon Monoxide / Q000378:metabolism*; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000009:adverse effects; D004791:Enzyme Inhibitors / Q000008:administration & dosage; D006419:Heme Oxygenase (Decyclizing) / Q000037:antagonists & inhibitors / Q000378:metabolism; D007275:Injections, Intravenous; D007276:Injections, Intraventricular; D053583:Interleukin-1beta / Q000008:administration & dosage; D008297:Male; D009490:Neurosecretory Systems / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D013312:Stress, Physiological / Q000187:drug effects; D013315:Stress, Psychological / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors
chemical_list: D004791:Enzyme Inhibitors; D053583:Interleukin-1beta; D009569:Nitric Oxide; D002248:Carbon Monoxide; D000324:Adrenocorticotropic Hormone; D019001:Nitric Oxide Synthase; D006419:Heme Oxygenase (Decyclizing)