Nitric oxide (NO) is now well characterised as a physiologically important molecule, acting most notably as an intra- and intercellular messenger within the cardiovascular and nervous systems.1 To fulfil these functions NO is produced in a tightly controlled manner by calcium dependent, constitutively expressed nitric oxide synthases (cNOS) present within endothelial and neural cells. Under pathological conditions, however, NO acts very differently from a benign signalling molecule. In these circumstances NO is produced in large, apparently tissue damaging amounts by inducible, calcium unregulated nitric oxide synthases (iNOS). For example, in inflammatory bowel disease the presence of high local concentrations of pro-inflammatory cytokines, such as interleukin 8, is associated with the induction of iNOS and so the continuous local generation of NO,2 ,3 possibly in very great amounts.4 Notably, this difference in NO production between cNOS and iNOS enzymes is not due, as is often remarked, to the inducible isoform of NO synthase being capable of producing more NO than the constitutive forms. Indeed, cNOS and iNOS enzymes function with very similar kinetics, co-factor requirements and substrate affinities. The important …