Nitric oxide (NO) is a messenger molecule with diverse functions throughout the body. In the brain and peripheral nervous system, NO displays many properties of a neurotransmitter and may be involved in long term potentiation. It is implicated in neurotoxicity associated with stroke and neurodegenerative diseases, neural regulation of smooth muscle, including peristalsis, and penile erection. NO is also responsible for endothelium-derived relaxing factor activity regulating blood pressure. In macrophages, NO mediates tumoricidal and bactericidal actions, as indicated by the fact that inhibitors of NO synthase (NOS) block these effects. Neuronal NOS and macrophage NOS are distinct isoforms.[3] Both the neuronal and the macrophage forms are unusual among oxidative enzymes in requiring several electron donors: FAD, flavin mononucleotide (FMN), NADPH, and tetrahydrobiopterin.[4]
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^Winkelmann J, Lichtner P, Schormair B, Uhr M, Hauk S, Stiasny-Kolster K et al. (February 2008). "Variants in the neuronal nitric oxide synthase (nNOS, NOS1) gene are associated with restless legs syndrome". Mov. Disord.23 (3): 350–8. doi:10.1002/mds.21647. PMID18058820.
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^ abJaffrey SR, Snowman AM, Eliasson MJ, Cohen NA, Snyder SH (January 1998). "CAPON: a protein associated with neuronal nitric oxide synthase that regulates its interactions with PSD95". Neuron20 (1): 115–24. doi:10.1016/S0896-6273(00)80439-0. PMID9459447.
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Further reading
Miyagoe-Suzuki Y, Takeda SI (2001). "Association of neuronal nitric oxide synthase (nNOS) with alpha1-syntrophin at the sarcolemma". Microsc. Res. Tech.55 (3): 164–70. doi:10.1002/jemt.1167. PMID11747091.