Abstract
Nitric oxide (NO), an atmospheric gas, is now known to be enzymatically synthesized in a tightly regulated manner by a number of tissues and cell types. Over the past 5 years, significant progress has been made elucidating the mechanism of NO synthesis and the functions of NO in different biological systems. NO is produced by cells, and serves a wide variety of functions in different cells, ranging from vascular endothelia, immune cells, neurons and glia, hepatocytes and smooth muscle cells (reviewed in: 1–3). The functions of NO appear very diverse, having actions on vascular tone, neurotransmission (2), immune cytotoxicity (3,4), and many others. Three isoforms of NO synthase (NOS) have been identified as being responsible for this synthesis in the presence of oxygen, NADPH and flavins, and represent three distinct gene products (1). Two of the enzyme types are continuously present and, thus are termed constitutive NOS. The first, termed NOS-I is found in the cytosol of central and peripheral neurons (2), and the second (NOS-III) was originally expressed by the vascular endothelium. Small amounts of NO are generated by these two iso-enzymes when they are activated by the calcium/calmodulin complex. In contrast, NOS-II, or inducible NOS, is expressed in many cell types after challenge by immunological or inflammatory stimuli (3). This isoform, the activity of which is independent of calcium and calmodulin, generates large amounts of NO over longer periods which are dependent on the presence of the stimuli.
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Goureau, O., Becquet, F., Courtois, Y. (1995). Nitric Oxide in the Retina. In: Anderson, R.E., LaVail, M.M., Hollyfield, J.G. (eds) Degenerative Diseases of the Retina. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1897-6_7
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DOI: https://doi.org/10.1007/978-1-4615-1897-6_7
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