Neuronal nitric oxide synthase effects

In the rat retina, ischemia upregulates expression of the neuronal nitric oxide synthase and cyclo-oxygenase-2 these effects can be effectively inhibited by lutein (Choi et al., 2006). 

Cavas, M. Navarro, J. F. (2006). Effects of selective neuronal nitric oxide synthase inhibition on sleep and wakefulness in the rat. Prog. Neuropsychopharmacol. Biol. Psychiatry 30, 56-67. 

Dzoljic, E., van Leeuwen, R., de Vries, R. Dzoljic, M. R. (1997). Vigilance and EEC power in rats effects of potent inhibitors of the neuronal nitric oxide synthase. Naunyn Schmiedebergs Arch. Pharmacol. 356, 56-61. 

AC VIII, adenylyl cyclase type VIII BDNF, brain-derived neurotrophic factor CamKII, calcium-calmodulin kinase II GIRK2, G protein-activated inward rectifying potassium 2 MAOA, monoamine oxidase A n.d., not determined NCAM, neural cell adhesion molecule nNOS, neuronal nitric oxide synthase Petl, ETS domain transcription factor tPA, serine protease tissue-plasminogen activator (tPA). t/ > Increase/decrease in anxiety-related behavior. No effect. 

Bird, D. C., Bujas-Bobanovic, M., Robertson, H. A., Dursun, S. M. Lack of phencyclidine-induced effects in mice with reduced neuronal nitric oxide synthase, Psychopharmacology 2001, 155, 299-309. 

Huang, Z., Huang, P.L., Panahian, N., Dalkara, T., Fishman, M.C., Moskowitz, M.A. Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase, Science 1994, 265, 1883-1885. 

Poux JM, Lartigue M, Chaisemartin RA et al. (1995) Uraemia is necessary for erythropoietin-induced hypertension in rats. Clin Exp Pharmacol Physiol 22 769-771 Roczniak A, Fryer JN, Levine DZ, Burns KD (1999) Downregulation of neuronal nitric oxide synthase in the rat remnant kidney. J Am Soc Nephrol 10 704-713 Santos F, Chan JCM, Hanna JDetal. (1992) The effect of growth hormone on the growth failure of chronic renal failure. Pe-diatr Nephrol 6 262-266... 

Wolthers, Kirsten R., Schimerlik, Michael I. (2002) Neuronal nitric oxide synthase substrate and solvent kinetic isotope effects on the steady-state kinetic parameters for the reduction of 2, 6-dichloroindophenol and cytochrome C3+, Biochemistry 41, 196-204. 

The influence of neuronal nitric oxide synthase (nNOS) on renal arteriolar tone has been studied in the perfused juxtamedullary nephron preparation [126]. Superfusion with a specific nNOS inhibitor decreased afferent and efferent arteriolar diameters, and these decreases in arteriolar diameters were prevented by interruption of distal volume dehvery by papillectomy. When volume delivery to the macula densa segment was increased, afferent arteriolar vasoconstrictor responses to the nNOS inhibitor were enhanced, but this effect was again completely prevented after papillectomy. In contrast, the arteriolar diameter responses to a nonselective NOS inhibitor were only attenuated by papillectomy. Specific nNOS inhibition enhanced the efferent arteriolar vasoconstrictor response to ANG II but did not alter the afferent arteriolar vasoconstrictor responsiveness to ANG II. In contrast, non specific NOS inhibition enhanced both afferent and efferent arteriolar vasoconstrictor responses to ANG It. This study demonstrates that the modulating influence of nNOS on afferent arteriolar tone of juxtamedullary nephrons is dependent on distal tubular fluid flow and that nNOS exerts a differential modulatory action on... 

Effects of cerebral ischemia in mice deficient in neuronal nitric oxide synthase. Science 265, 1883-1885. 

Watanabe H, Muramatsu Y, Kurosaki R et al. Proteotive effects of neuronal nitric oxide synthase inhibitor in mouse brain against MPTP neurotoxicity an immunohistological study. Eur Neuropsychopharmacol 2004 14 93-104. 

Abu-Soud HM, Gachhui R, Raushel FM, Stuehr DJ (1997) The ferrous-dioxy complex of neuronal nitric oxide synthase. Divergent effects of i-arginine and tetrahydrobiopterin on its stability. J Biol Chem 272 17349-17353... 

Figure 1 Models for analyzing tissue PO2 disappearance rates measured with PO2 microelectrodes after stopping perfusate flow to the carotid body, (a) Inhibitory effects of NO on a single enzyme model for C3tiochrome oxidase (high-affinity pathway) are shown, based on a decrease in maximum tissue PO2 disappearance rate (top panel) and increase in (middle panel) with NO. Predicted 02-dependent PO2 disappearance rates (bottom panel) for NO concentrations of 0 (circle), 100 (triangle). 250 (diamond), and 500 nM (square) are shown, (b) The single-oxidase model was modified by adding a second, low-affinity (high enzyme (top panel) for 02-dependent production of NO by neuronal nitric oxide synthase (nNOS). Predicted 02-dependent PO2 disappearance rates (bottom panel) are shown with the additional amount of O2 consumed by the low-affinity pathway (dashed lines) over that required by the high-affinity pathway (solid lines) for each NO concentration (symbols same as above).

In the developing rat, the facilatory effect of intermittent hypoxia has been shown to be manifest as a reduction in hypoxic ventilatory decline observed with continuous hypoxia. This phenomenon was abolished by administrations of 7-nitroindazole, an antagonist of neuronal nitric oxide (NO) synthase, leading to the conclusion that this manifestation of the facilatory effect of chronic intermittent hypoxia is mediated by enhanced expression of neuronal NO (50). On the other hand, mutant mice deficient in neuronal nitric oxide synthase manifest augmented hypoxic responses (55). Whether the locus of this modulation is peripheral or central is unclear. 

Zhu Y, Jones G et al (2005) Lentivirus infection causes neuroinflammation and neuronal injury in dorsal root ganglia pathogenic effects of STAT-1 and inducible nitric oxide synthase. J Immunol 175(2) 1118-1126... 

---