Although its discovery as a biological mediator only dates back about 15 years, nitric oxide (NO) is now widely recognized by every biologist or biochemist as a ubiquitous mediator in diverse biological processes in nearly all aspects of life. Among the classic actions of NO are regulation of vascular and bronchial tone, neurotransmission, antimicrobial activity, and modulation of inflammatory-immune processes (1-3). Considerable interest has been devoted to the involvement of NO in inflammation, since its production is usually dramatically increased under infectious or inflammatory conditions to provide a host defense mechanism and/or regulate the progression of inflammatory-immune processes. Many investigations have, however, insinuated that overproduction of NO can also directly provoke detrimental conditions and contribute to the pathobiology of inflammatory diseases. It is generally assumed that such adverse actions of NO are attributed to accelerated metabolism of NO to more reactive nitrogen intermediates, due to the presence of oxidant-producing mechanisms. The multiple and often paradoxical biological effects of NO form one of the major unsolved controversies in the inflammationrelated diseases and have impeded efforts to implicate NO as a therapeutic target in these conditions.
|Original language||English (US)|
|Title of host publication||Therapeutic Targets in Airway Inflammation|
|Number of pages||22|
|State||Published - Jan 1 2003|
ASJC Scopus subject areas