NO has a short half-life due to its reactivity and therefore diffuses only short distances. NO can rapidly move from cell to cell independent of membrane channels or receptors and react with a wide array of molecular targets. In contrast, the sustained production of NOS-2 generated NO contributes to antimicrobial activities, tissue injury, or conversely tissue protection depending on the setting. This basal release also reduces the adhesion of platelets and polymorphonuclear granulocytes (PMN) to the endothelium. The basal release of NOS-3 generated NO maintains vasodilation in small resistance arteries in part through the guanylate cyclase/cGMP system in smooth muscle cells, leading to relaxation of the vessel wall. While NOS-3 is expressed in a limited number of cells, NOS-2 can be expressed in a wide variety of cell types, and its expression is regulated at tile level of transcription and iNOS mRNA stability. NOS-2 differs considerably in its pattern of expression and regulation than the constitutive isoforms.
endotoxin, peptidoglycan, lipoteichoic acid), or hypoxia, constitutive NOS-2 expression has been observed in lung and small bowel epithelial cells. NOS-2 typically only is expressed when cells are exposed to proinflammatory cytokines, microbial products (i.e. The constitutive NO synthases (NOS 1 and NOS 3) produce NO in small amounts whereas the inducible NOS is responsible for the production of large amounts of NO. Three isoforms have been described and cloned ( 1): endothelial cell NOS (ecNOS, or type 3), brain NOS (bNOS, nNOS, or type 1), and inducible macrophage type NOS (iNOS, or type 2). The free radical nitric oxide (NO) is synthesized from one of the two chemically equivalent guanidino groups of L-arginine and oxygen by a family of enzymes termed NO synthases (NOS).
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