Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.5.1.19 (NOS)
7,285 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of nicotinamide adenine dinucleotide phosphate-diaphorase (or -dehydrogenase, NADPHDH, a marker for nitric oxide synthase, NOS) positive neurons was demonstrated histochemically in the central nervous system of the swordtail fish Xiphophorus helleri, a highly derived telost of the atherinomorph outgroup. All nuclei of the swordtail fish, comprising almost all nuclei that have been described so far regarding the brains of telosts in general, were investigated. The results obtained clearly indicate, that NADPHDH positive neurons in the swordtail fish mostly are restricted to evolutionary primitive brain areas such as to most dorsomedial, dorsocentral and ventral portions of the telencephalon, to the preoptic area and to some thalamic, hypothalamic and pretectal nuclei of the diencephalon including the pituitary and the pineal organ, to the nuclei of the mesencephalic and myelencephalic cranial nerves, to the myelencephalic reticular formation and to the Mauthner cells. Some positive neurons were also observed within the mesencephalon, including the cerebellar body and its valve. Among non-neuronal cells, especially ependymocytes were strongly stained. It is the particular goal of the present study to provide a complete account on NADPHDH in the brain of a fish species, since, firstly, the NADPHDH/NOS system becomes increasingly important with regard to the understanding of the molecular basis of memory formation, and, secondly, fishes generally are more and more intensively studied concerning neurobiological approaches.
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PMID:An atlas of the distribution of NADPH-diaphorase in the brain of the highly derived swordtail fish Xiphophorus helleri (Atherinoformes:Teleostei). 887 64

Endothelial Nitric Oxide Synthase (eNOS) mediates the conversion of L-argine to NO and citrulline, which requires Nicotinamide Adenine Dinucleotide Phosphate (NADPH) as an essential cofactor. Evidence has been given that NOS accounts for the NADPH-diaphorase activity. The aim of the present study was to identify the histochemical and immunocytochemical appearance of NADPH-diaphorase and von Willebrand factor (factor VIII) respectively, in endothelial cells (ECs) during healing of stretch-expanded polytetrafluoroethylene (ePTFE) arterial grafts. On six Swedish domestic pigs an iliac bypass was bilaterally performed using 6 mm stretch-ePTFE grafts. The animals were allowed to survive one, two or four weeks. After explanation the grafts were prepared for NADPH-diaphorase histochemistry and factor VIII immunohistochemistry. Positive staining for the two identification markers was demonstrated after two weeks, whereas a more intense staining was seen after four weeks at the proximal and distal anastomoses, indicating maturation by time. No stained cells were observed at the mid-region of the grafts at any time. The cells differed from normal ECs, the former being less intense which may reflect immature ECs and probably a decreased expression of NO. In conclusion, the present study suggests tha NADPH-d histochemistry can be used to identify ECs. Whether a lower expression of NO compared to normal cells also means a reduced function, capable of causing adverse events has to be further evaluated.
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PMID:NADPH-diaphorase expression of endothelial cells during four weeks' healing of a stretch-ePTFE graft: an experimental porcine study. 897 80

There is increasing evidence that carbon monoxide (CO), like nitric oxide (NO), may be a neuronal messenger molecule. This study investigated the expression of heme oxygenase-2 (HO-2), the enzyme responsible for the synthesis of CO, by intracardiac neurones. Many, if not all newborn guinea-pig intracardiac neurones in culture were HO-2-immunoreactive. Furthermore, double labelling showed that a relatively small subpopulation of these neurones also expressed NO synthase/nicotinamide dinucleotide phosphate (NADPH)-diaphorase (NOS/NADPH-d) activity. These findings suggest that intracardiac neurones can synthesize CO and that CO may be fundamental to their function. Comparison of the proportions of intracardiac neurones that contain HO-2 with those that express NOS/NADPH-d activity also indicates that CO may be more important than NO in the intrinsic neuronal control of the heart.
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PMID:Heme oxygenase-2 and nitric oxide synthase in guinea-pig intracardiac neurones. 914 Oct 89

The small subpopulation of striatal neurons containing nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d, recently identified as nitric oxide synthase, NOS) is selectively spared in Huntington's disease. Previous search for pathogenic mechanisms capable of destroying striatal neurons but sparing NADPH-d(+) cells has identified only NMDA receptor-mediated excitotoxicity. In view of suggestions that neuronal death in Huntington's disease may occur by apoptosis, we examined the vulnerability of NADPH-d(+) neurons to apoptosis. Murine striatal or cortical cultures exposed to serum deprivation developed extensive neuronal apoptosis, but NADPH-d(+) neurons were relatively spared. This sparing was seen when cultures were exposed to several other apoptosis-inducing insults. It was not seen after toxic exposure to H2O2, and it was not blocked by NOS inhibition. The selective resistance of NADPH-d(+) neurons to several forms of apoptosis provides key support for the possibility that apoptosis may contribute to the pathogenesis of Huntington's disease.
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PMID:NADPH diaphorase-containing striatal or cortical neurons are resistant to apoptosis. 917 14

The distribution of nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) reactivity and neuronal nitric oxide synthase immunoreactivity (nNOS-IR) was investigated in the rat retina during photoreceptor regeneration. Photoreceptor damage and the disappearance of a NADPHd reactive/nNOS-IR band corresponding to inner photoreceptor segments were observed after continuous exposure to light irradiation. Both events were reversible after 20 days of total darkness. Also a progressive decrease in the number and in the staining intensity of NADPHd reactivity in amacrine cells were found along the first 3-6 days of darkness stabilizing thereafter in both illuminated and control groups. However, staining intensity in the former group remained more elevated than in the latter one. NOS activity in the retina varies depending on functional and pathological states.
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PMID:Changes in NADPH diaphorase reactivity and neuronal nitric oxide synthase in the rat retina following constant illumination. 928 Jan 64

Nitric oxide (NO) production by macrophages is mainly regulated by induction of nitric oxide synthase (iNOS) by cytokines and microbial products. Nicotinamide (NIC) inhibits NO production by activated macrophages in a dose dependent manner. NIC also inhibits NOS enzyme activity in extracts from activated macrophages. The inhibition was noncompetitive with L-arginine (Ki 13.37 +/- 4.40 mM, n=3), uncompetitive versus NADPH (Ki 3.06 +/- 0.17 mM, n=3) and tetrahydrobiopterin. Finally, the inhibition by nicotinamide was fully reversed by scavenging NO with hemoglobin. We suggest that NIC acts by allowing NO to inhibit its own formation.
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PMID:Nicotinamide inhibits inducible nitric oxide synthase enzyme activity in macrophages by allowing nitric oxide to inhibit its own formation. 936 31

During our studies on the multiple possible functions of nitric oxide (NO) in chick retinal development and physiology, we have demonstrated the presence and the activity of NO synthase (NOS-I and III) in certain neuronal populations (photoreceptors, amacrine cells in the inner nuclear and ganglion cells) and also in synaptic-rich regions in the developing chick retina. Both enzymes, detected by nicotinamide adenine dinucleotide phosphate (NADPH)-diaphorase, immunohistochemistry and Western blotting, appeared between embryonic days 6 and 12, and followed a spatial and temporal pattern of expression which correlated with the differentiation of the neuronal layers. Evaluation of the conversion of [3H]-labeled arginine to [3H]-citrulline, confirmed the presence of a calcium-dependent NOS activity in the cytosolic and particulate retinal extracts during the development. This pattern of NOS expression suggests that the regulated release of NO during key phases of development might be one mechanism involved in the regulation of retinal differentiation.
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PMID:Developmental expression of nitric oxide synthase isoform I and III in chick retina. 937 86

The distribution of immunoreactivity to neuronal nitric oxide synthase (nNOS) and vasopressin (AVP) was studied in the circumventricular organs of the female rat. The occurrence of NOS immunoreactivity showed correspondence to nicotinamide dinucleotide phosphate diaphorase reactivity, a previously used but less specific marker for neuronal NOS. nNOS immunolabeling was detected in the two most rostrally located circumventricular organs - the organum vasculosum of the lamina terminalis and the subfornical organ. In the latter, AVP immunoreactivity was observed in some cell bodies, which also were nNOS-immunoreactive. In the median eminence and the neurohypophysis there were large amounts of nNOS- and AVP-immunoreactive nerve fibers, which often displayed similarities in distribution and morphology. Within the pineal gland, only very few nNOS-immunoreactive varicose terminals were observed, which ran along blood vessels. nNOS immunoreactivity was also seen in the epithelium of the choroid plexus, whereas no nNOS immunoreactivity could be found in the subcommissural organ or in the area postrema. The present demonstration of nNOS and AVP immunoreactivity in the subfornical organ, median eminence, and neurohypophysis, and the occurrence of nNOS immunoreactivity also in the choroid plexus and organum vasculosum of the lamina terminalis, provides a morphological background for a functional role for nitric oxide in water homeostatic mechanisms, both as executed through the hypothalamohypophyseal system and via the production of cerebrospinal fluid.
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PMID:Nitric oxide synthase and vasopressin in rat circumventricular organs. An immunohistochemical study. 938 4

The possible localization of nitric oxide (NO) synthase (NOS) in proximity to the microvasculature was examined in the rat adenohypophysis using immunohistochemistry and nicotinamide adenine dinucleotide phosphate diaphorase histochemistry. A population of NOS-positive cells was localized in very close contact with the sinusoidal capillaries. The pattern of this perivascular localization was either unicellular, bicellular or multicellular. These observations suggest that, at least, some actions of NO in the adenohypophysis can be accounted for by a local regulation of the glandular microvasculature.
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PMID:Perivascular localization of nitric oxide synthase in the rat adenohypophysis: potential implications for function and cell-cell interaction. 951 79

Angiotensin type-1a (AT1a) receptor gene-knockout (AT1a-/-) mice exhibit chronic hypotension and renin overproduction. In the kidneys of AT1a-/- mice, the activity of neuronal type nitric oxide synthase (N-NOS) was histochemically detected by nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase (NADPHd) reaction combined with N-NOS immunohistochemistry. The localization of renin was detected by immunohistochemistry and the results were analyzed morphometrically. The levels of N-NOS and renin mRNA in the renal cortical tissue were determined by reverse transcription-PCR and Northern blot analysis, respectively. In the renal sections from wild-type mice, NADPHd activity and N-NOS immunoreactivity were localized to the discrete region of the macula densa in contact with the parent glomerulus. In contrast, N-NOS-positive macula densa cells were distributed beyond the original location of the macula densa, occasionally extending to the opposite side of the distal tubules. The mean number of N-NOS positive macula densa cells was significantly increased in AT1a-/- mice (186 per 100 glomeruli) compared with wild-type mice (65 per 100 glomeruli). AT1a-/- mice showed 1.4-times higher N-NOS mRNA levels in the renal cortical tissues than wild-type mice. The plasma renin activity was significantly higher in AT1a-/- mice (205.5 +/- 26.1 ng/ml/hr) than in wild-type mice (8.0 +/- 0.2 ng/ml/hr). The renin-positive areas per glomerulus and renal renin gene expression were 12-times and 2.6-times higher in AT1a-/- mice than in wild-type mice, respectively. These abnormalities, however, were less remarkable in AT1a-/- mice compared with angiotensinogen-knockout mice. When AT1a-/- mice were fed a high-salt diet, the signal intensity of the NADPHd reaction and the number of positively-stained macula densa cells were significantly decreased. The levels of renal cortical N-NOS mRNA were also suppressed by the treatment. Dietary salt loading produced a parallel decrease in plasma renin activity, renal renin-immunoreactive areas, and the levels of renin mRNA without affecting systemic blood pressure. These results provide evidence for the possible involvement of N-NOS at the macula densa in the increased renin production in AT1a-/- mice.
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PMID:Expression of neuronal type nitric oxide synthase and renin in the juxtaglomerular apparatus of angiotensin type-1a receptor gene-knockout mice. 960 88


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