Nitric oxide transport and storage in the cardiovascular system.

Despite short halflife in biological fluids, nitric oxide (NO) can produce remote or long lasting effect in the cardiovascular system. Long distance transport or local storage of NO might explain these effects. In blood, recent findings suggest that in addition to being a major consumption pathway, interaction of NO with hemoglobin may permit O(2)-governed transport of NO (as S-nitrosohemoglobin) to tissues in which NO may be released together with O(2), via transnitrosation of a transport protein. In blood vessels, two different putative NO stores have been characterized. The first is the photosensitive store, formed from endothelium-derived NO. The mechanism of NO release from this store in the body (in absence of light) and its physiological relevance are unknown. The second store is generated in conditions of high tissue NO levels, as a consequence of the inducible NO synthase activity or in various stress conditions. This NO store involves formation of protein-bound dinitrosyl iron complexes or S-nitrosated proteins, or both. Low molecular weight thiols can displace NO from these stores and probably transfer it to target membrane protein(s) such as K(+) channels, via transnitrosation reactions. These stores may be involved in defence mechanisms against inflammation or stress. Thus, NO transport and storage mechanisms may be implicated in a variety of NO effects. The mechanisms of their formation and of NO release and their physiologic and pathophysiologic relevance deserve further investigations.