Nitric oxide diffusion

Nitric oxide diffuses into the cell and directly activates a soluble, cytoplasmic guanylate cyclase, so no receptor or G protein is required. 

Red blood cells typically contain 20 mM oxyhemoglobin and thus will destroy nitric oxide diffusing into the vascular stream. Nitric oxide can diffuse over... 

In blood-containing vascular beds, the inactivation of nitric oxide by oxygen is of minor importance because of the rapid and irreversible reactions of nitric oxide with oxyhemoglobin in red blood cells. Any nitric oxide that diffuses into the vascular lumen will be quickly destroyed, making blood vessels effective sinks for nitric oxide. The half-life of nitric oxide is sufficiently long that nitric oxide diffusing into the vascular smooth muscle could also diffuse back out to the lumin to be inactivated by hemoglobin in red blood cells. 

FIGURE 2 Peroxynitrite (ONOO )-induced loss of nitric oxide signal. A saturated aqueous solution (0.5 jul) of nitric oxide (1.9 mM) was added to a stirred 1-ml solution of 0.1 M potassium phosphate (pH 7.4) at 37°C. ONOO" was added at the times indicated. ONOO" (40 /U.M) was allowed to decompose at pH 7.4 for 1 min prior to addition. Nitric oxide diffused through a hollow fiber immersed in the solution and was carried to a chemiluminescence detector by a helium flow. The dead time for measurement of nitric oxide added to the solution is approximately 1 sec. 

Rubbo, H., C. Batthyany, B. A. Freeman, R. Radi, and A. Denicola. 1998. Nitric oxide diffusion across low density lipoprotein and inhibition of bpid oxidation-dependent chemiluminescence. Nitric Oxide 2 (supp. 2) 117. 

Keh, D., Gerlach, M., Kurer, I., Spiehnann, S., Kemer, T., Busch, T., Hansen, R., Falke, K., Gerlach, H., 1999. Nitric oxide diffusion across membrane lungs protects platelets during simulated extracorporeal circulation. European Journal of Chnical Investigation 29,344—350. 

Nitric Oxide. Nitric oxide [10102-43-9] NO, is a ubiquitous intracellular and intercellular messenger serving a variety of functions including vasodilation, cytotoxicity, neurotransmission, and neuromodulation (9). NO is a paramagnetic diatomic molecule that readily diffuses through aqueous and hpid compartments. Its locus of action is dictated by its chemical reactivity and the local environment. NO represents the first identified member of a series of gaseous second messengers that also includes CO. 

The results of a number of studies demonstrate that the gas nitric oxide (NO) plays a functional role in the central nervous system. This all originated with the discovery that the so-called endothelium-derived relaxing factor (EDRF), found in blood vessels, and thought to be a peptide, was in fact NO. The potential roles of this freely diffusible gas have subsequently been extended to many other tissues and organs but we will concentrate on the possible neuronal roles of what is obviously a novel mediator. There are also suggestions that the closely related carbon monoxide may also have a function in the central nervous system. 

Figure 13.9 The production and actions of nitric oxide (NO). The influx of calcium through either calcium channels or NMDA receptors triggers NOS to convert L-arginine to NO. L-NAME and 7-NI inhibit this process. NO, once produced, can diffuse in a sphere and then can activate guanylate cyclase...

Marino, J. Cudeiro, J. (2003). Nitric oxide-mediated cortical activation a diffuse wake-up system. J. Neurosci. 23, 4299-307. 

The book focuses on three main themes catalyst preparation and activation, reaction mechanism, and process-related topics. A panel of expert contributors discusses synthesis of catalysts, carbon nanomaterials, nitric oxide calcinations, the influence of carbon, catalytic performance issues, chelating agents, and Cu and alkali promoters. They also explore Co/silica catalysts, thermodynamic control, the Two Alpha model, co-feeding experiments, internal diffusion limitations. Fe-LTFT selectivity, and the effect of co-fed water. Lastly, the book examines cross-flow filtration, kinetic studies, reduction of CO emissions, syncrude, and low-temperature water-gas shift. 

Reaction of nitric oxide with superoxide is undoubtedly the most important reaction of nitric oxide, resulting in the formation of peroxynitrite, one of the main reactive species in free radical-mediated damaging processes. This reaction is a diffusion-controlled one, with the rate constant (which has been measured by many workers, see, for example, Ref. [41]), of about 2 x 109 1 mol-1 s-1. Goldstein and Czapski [41] also measured the rate constant for Reaction (11) ... 

Simultaneous generation of nitric oxide and superoxide by NO synthases results in the formation of peroxynitrite. As the reaction between these free radicals proceeds with a diffusion-controlled rate (Chapter 21), it is surprising that it is possible to detect experimentally both superoxide and NO during NO synthase catalysis. However, Pou et al. [147] pointed out that the reason is the fact that superoxide and nitric oxide are generated consecutively at the same heme iron site. Therefore, after superoxide production NO synthase must cycle twice before NO production. Correspondingly, there is enough time for superoxide to diffuse from the enzyme and react with other biomolecules. 

As mentioned earlier, ascorbate and ubihydroquinone regenerate a-tocopherol contained in a LDL particle and by this may enhance its antioxidant activity. Stocker and his coworkers [123] suggest that this role of ubihydroquinone is especially important. However, it is questionable because ubihydroquinone content in LDL is very small and only 50% to 60% of LDL particles contain a molecule of ubihydroquinone. Moreover, there is another apparently much more effective co-antioxidant of a-tocopherol in LDL particles, namely, nitric oxide [125], It has been already mentioned that nitric oxide exhibits both antioxidant and prooxidant effects depending on the 02 /NO ratio [42]. It is important that NO concentrates up to 25-fold in lipid membranes and LDL compartments due to the high lipid partition coefficient, charge neutrality, and small molecular radius [126,127]. Because of this, the value of 02 /N0 ratio should be very small, and the antioxidant effect of NO must exceed the prooxidant effect of peroxynitrite. As the rate constants for the recombination reaction of NO with peroxyl radicals are close to diffusion limit (about 109 1 mol 1 s 1 [125]), NO will inhibit both Reactions (7) and (8) and by that spare a-tocopherol in LDL oxidation. 

Activation of brain H receptors also stimulates cGMP synthesis [19]. Outside the brain, histamine is known to relax vascular smooth muscle by activation of endothelial H receptors, thereby increasing endothelial Ca2+ concentrations and stimulating the synthesis and release of nitric oxide. The latter, a diffusible agent, then activates the smooth muscle guanylyl cyclase [30]. Although less is known about these mechanisms in the CNS, there is evidence that brain H receptor activation can produce effects that depend on guanylyl cyclase activity [19]. 

Although NO does not itself use a G-protein for signalling, the mechanism of NO production in vascular endothelium is initiated by IP3 via a G-protein-linked acetylcholine receptor on the cell surface. The IP3 causes activation of nitric oxide synthase via calcium- calmodulin and the NO generated diffuses from the endothelial cell into the adjacent smooth muscle cell where cGMP is produced. 

The relative importance of these three mechanisms in NO formation and the total amount of prompt NO formed depend on conditions in the combustor. Acceleration of NO formation by nonequilibrium radical concentrations appears to be more important in non-premixed flames, in stirred reactors for lean conditions, and in low-pressure premixed flames, accounting for up to 80% of the total NO formation. Prompt NO formation by the hydrocarbon radical-molecular nitrogen mechanism is dominant in fuel-rich premixed hydrocarbon combustion and in hydrocarbon diffusion flames, accounting for greater than 50% of the total NO formation. Nitric oxide formation by the N20 mechanism increases in importance as the fuel-air ratio decreases, as the burned gas temperature decreases, or as pressure increases. The N20 mechanism is most important under conditions where the total NO formation rate is relatively low [1],... 

Reiativeiy recentiy, the gases nitric oxide (NO) and carbon monoxide (CO) have been found to act as neurotransmitters in the nervous system. Nitric oxide is synthesized from L-arginine via nitric oxide synthase, requiring NADPH as a co-enzyme and tetrahydrobiopterin as a cofactor. Unlike other neurotransmitters, NO is a smaii, very soiubie moiecuie and cannot be stored in synaptic vesicles. Rather, it is synthesized on demand and freeiy diffuses through membranes. It is not broken down enzymaticaiiy because it is unstabie and degrades rapidiy. NO may have several actions, one of which is to increase the production of cGMP by guanyiyi... 

Nitric oxide (NO) is synthesized by vascular endothelium in response to vasodilators. It diffuses into the surrounding vascular smooth muscle, where it directly binds the heme group of soluble guanylate cyclase, activating the enzyme. 

Gifford and Hanna tested their simple box model for particulate matter and sulfur dioxide predictions for annual or seasonal averages against diffusion-model predictions. Their conclusions are summarized in Table 5-3. The correlation coefficient of observed concentrations versus calculated concentrations is generally higher for the simple model than for the detailed model. Hanna calculated reactions over a 6-h period on September 30, 1%9, with his chemically reactive adaptation of the simple dispersion model. He obtained correlation coefficients of observed and calculated concentrations as follows nitric oxide, 0.97 nitrogen dioxide, 0.05 and rhc, 0.55. He found a correlation coefficient of 0.48 of observed ozone concentration with an ozone predictor derived from a simple model, but he pointed out that the local inverse wind speed had a correlation of 0.66 with ozone concentration. He derived a critical wind speed formula to define a speed below which ozone prediction will be a problem with the simple model. Further performance of the simple box model compared with more detailed models is discussed later. 

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