N itric oxide synthesized by endothelial NO synthase (eNOS) is a principal mediator of smooth muscle relaxation in the normal blood vessel. With inflammation, however, inducible NO synthase (iNOS) is expressed in the vessel wall, including the adventitia, 1 and is associated with impaired endothelium-dependent vasorelaxation 2 and impaired vasoconstriction. 3,4 The molecular mechanism(s) underlying these alterations in vasomotor function accompanying inflammation remains unknown, although in

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... ro studies suggest that proinflammatory stimuli reduce the expression of eNOS, agonist-mediated cytosolic calcium mobilization, and NO production. 5