Cross-talk between constitutive and inducible nitric oxide synthases.

Abstract

To the Editor, We read with great interest the recent work by Kanno et al1 describing the protective effect of nitric oxide (NO) against myocardial ischemia/reperfusion injury and were struck by the other phenomenon associated with it: superinduction of inducible NO synthase (iNOS) in endothelial NO synthase (eNOS) knockout mice. Although the exact mechanism is unknown and apparently “paradoxical,” the absence of constitutive NO seems to increase inducible NO production. In this respect, the authors argued that the effect could be due to redox stress associated with the absence of NO. Recently, we published an article2 suggesting cross-talk between constitutive and inducible NOS using NO as a modulator. In particular, low (ie, physiological) NO levels inhibit iNOS transcription by inactivating nuclear factor-κB (NF-κB).3 4 5 However, when NO levels decrease beneath a putative threshold value (eg, as …