Abstract
Oxygen is a critical substrate for both nitric oxide (NO) and superoxide (02-) biosynthesis. Previous studies have established that constitutive calcium-dependent NO synthase (NOS) and 02 producing NADPH-oxidase are affected at the level of gene expression and at a functional level. For example, hypoxia increases expression of the genes encoding both macrophage and endothelial NOS isoforms, and low oxygen tension attenuates NOS activity and NO-dependent vascular relaxation. Both NOS and NADPH-oxidase participate in modulation of vascular tone ° although how oxygen regulates endothelial response is unclear. We have previously demonstrated the dependence of macrophage NADPH-oxidase on the cellular distribution of oxygen, and both superoxide and NO production by endothelial cells.
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Frenneaux, M.P., James, P.E., Parton, J., Jackson, S.K. (2003). Oxygen Indirectly Regulates Nitric Oxide Availability. In: Wilson, D.F., Evans, S.M., Biaglow, J., Pastuszko, A. (eds) Oxygen Transport To Tissue XXIII. Advances in Experimental Medicine and Biology, vol 510. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0205-0_23
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DOI: https://doi.org/10.1007/978-1-4615-0205-0_23
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