Nitric oxide and wound healing: an update.

Abstract

Because of its gaseous qualities, nitric oxide (NO) may pass across membranes and has a relatively short half-life. The enzyme complex nitric oxide synthase (NOS) in humans is responsible for the production of NO. This complex is composed of three distinct homodimeric isoforms: (1) neuronal isoform (nNOS (or NOS I), 2) inducible isoform (iNOS (or NOS II), and 3) endothelial isoform (eNOS/NOS III). L-arginine serves as the substrate for all NO isoforms, while molecular oxygen and NADPH serve as co-substrates. nNOs isoforms are expressed in specific neurons of the central nervous system and are involved in the regulation of blood pressure and synaptic plasticity. Endothelial cells are the primary source of the eNOS isoform, which plays a role in vasodilation, blood pressure regulation, and anti-atherosclerotic and vasoprotective effects. The inducible iNOS isoform is activated in response to stress; inflammatory cytokines, apoptotic bodies, or bacterial antigens induce an increase in enzyme expression.