Abstract
Nitric oxide (NO), a free radical gas messenger in endothelial cells of blood vessels and in some central neurons (for references, Moncada et al., 1991) appears an interesting candidate to be considered in the mechanism of carotid body cells chemotransduction in view of its rapid inactivation by oxygen and by Superoxides. Nitric oxide synthases (NOS) display close molecular homology with cytochrome P-450 reductase (Snyder, 1991). NOS molecule tightly bound with flavin adenine dinucleotide (FAD) transfers electrons successively between NADPH and flavins as a part of its catalytic activity (for references, Bredt et al., 1992). A similar molecular mechanism has been proposed as a molecular pathway of chemotransduction by Acker et al. (1992).
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Trzebski, A., Sato, A., Sato, Y., Suzuki, A. (1994). Carotid Chemoreceptor Activity and Heart Rate Responsiveness to Hypoxia After Inhibition of Nitric Oxide Synthase. In: O’Regan, R.G., Nolan, P., McQueen, D.S., Paterson, D.J. (eds) Arterial Chemoreceptors. Advances in Experimental Medicine and Biology, vol 360. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-2572-1_48
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DOI: https://doi.org/10.1007/978-1-4615-2572-1_48
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