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 objective of the study was to determine whether nitric oxide (NO) is present in clinically healthy horses (control) under basal conditions, and if it increases secondary to naturally acquired strangulating large colon volvulus (affected). Eleven affected horses and 10 controls were studied. Jugular venous blood, abdominal fluid, and urine were collected. The NO concentrations were standardized to the creatinine concentration in the respective samples. A biopsy specimen collected from the large colon pelvic flexure at surgery was divided into subsections for processing for inducible nitric synthase (iNOS) and nitrotyrosine (NT) immunohistochemical staining and reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemical staining. There were no significant differences in plasma, abdominal fluid, or urine NO concentrations between affected and control horses. There was a significant decrease in submucosal arteriolar and venular endothelium, submucosal plexus, mucosal leukocyte, mucosal and musclaris vasculature, and myenteric plexus NADPH diaphorase staining in affected versus control horses. There was a significant increase in iNOS staining in mucosal leukocytes and vasculature in affected versus control horses. Other than a greater number of positively stained mucosal leukocytes in affected horses, there were no significant differences between affected and control horses for NT staining. The presence of NADPH diaphorase staining in the endothelium and submucosal neurons suggests endothelial and neuronal NOS are present under basal conditions in the large colon of horses. Increased iNOS and NT staining in mucosal leukocytes of affected horses suggests involvement of the NO pathway in large colon volvulus. The reasons for the lack of a significant difference in plasma, abdominal fluid, and urine NO concentrations between affected and control horses are unknown.
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PMID:Detection and comparison of nitric oxide in clinically healthy horses and those with naturally acquired strangulating large colon volvulus. 1597 74

Maternal separation or social isolation is a risk factor in the development of mammalian species affecting both physical and mental growth, and food intake regulation. Melatonin has been known to regulate body weight on various species including rodents. We investigated the effect of melatonin treatment on the expression of nitric oxide synthase, which may involved in food intake regulation, in the brain of maternally separated-rats using nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Melatonin (10 mg/kg i.p.) was injected to 14-day-old maternally-separated rats for 7 days. Maternally-separated rats with melatonin administration showed significantly higher staining intensities of NADPH-d-positive neurons in the paraventricular nucleus (PVN) and in lateral hypothalamic area (LHA) than maternally-separated without melatonin administration (P < 0.05). Body weight of melatonin treated rats significantly increased at the 6th and 7th day compared to that of rats without melatonin treatment (P < 0.05). These results indicate that melatonin may be associated with increase body weight via NOS in the hypothalamic areas in maternally-separated or socially isolated rats.
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PMID:Melatonin enhances NADPH-diaphorase activities in the hypothalamus of maternally-separated rats. 1629 49

NO produced by endothelial NO synthase (NOS3) decreases sodium transport by the thick ascending limb (THAL). We found previously that 7 days of high salt (HS) increased THAL-NOS3 expression but not NO production. NOS3 phosphorylation regulates enzyme activity. We hypothesized that HS acutely increases NOS3 expression and NO production, and, over time, changes in NOS3 phosphorylation dissociate NO production from expression. NOS3 expression increased by 71+/-13%, 127+/-24%, and 69+/-16% at days 1, 3, and 7 of HS, respectively. At days 14 and 28, expression was back to normal salt. After 1 day of HS, NO production in response to 250 micromol/L L-arginine was elevated by 146% and, by day 3, returned to normal salt. Similar increases were found in response to endothelin-1. Inhibitors of NOS1/2 did not blunt the salt-induced increase in NO. Phosphorylation at Thr495, an inhibitory site, decreased by 39+/-8% at day 1 of HS and then increased by 116+/-18% at day 3. Phosphorylation at Ser633 and Ser1177 (stimulatory sites) decreased by &25% at day 1 and remained depressed at day 3. Superoxide production increased by 71% at day 1, decreased by 57% at day 3, and decreased by 55% at day 7. The NOS inhibitor L-NG-nitroarginine methyl ester did not alter superoxide levels at any time point. The addition of reduced nicotinamide-adenine dinucleotide phosphate and tetrahydrobiopterin had no effect on NO release after 3 days of HS. We conclude the following: (1) HS transiently increases NO production and NOS3 expression; (2) NOS3 expression and NO production are dissociated by HS; and (3) changes in phosphorylation explain how THAL NOS3 activity and expression are dissociated by HS.
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PMID:A high-salt diet dissociates NO synthase-3 expression and NO production by the thick ascending limb. 1634 77

The brainstem dorsal raphe nucleus (DRN) contains an abundant distribution of nitric oxide (NO) synthase (NOS)-containing neuronal profiles in two distinct populations: faint- and intense-immunoreactive cells in midline (ventromedial and dorsomedial) and lateral wing subregions, respectively. This study tested the hypothesis that different functional dynamics underlie the topography of NOS-containing cells in the DRN rostrocaudal and mediolateral neuraxis by using a capsaicin challenge paradigm (50 mg/kg, subcutaneous). Compared with vehicle, capsaicin significantly and preferentially increased nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d, an index of constitutive NOS) reactivity in the rostral midline and caudal lateral wing subregions. Furthermore, capsaicin activated more Fos-positive cells than vehicle within all subregions of the DRN but with a caudal versus rostral predominance in activation pattern. In addition, a high proportion of capsaicin-induced Fos cells in the midline but almost none in lateral wing stained for NADPH-d. These observations suggest the existence of two functionally distinct populations of NOS neurons in the DRN. Furthermore, capsaicin increased galanin immunoreactivity with predominant staining in cell soma and fiber processes in midline and lateral wing subregions of the nucleus, respectively. The total capsaicin-induced galanin immunoreactivity was higher in rostral versus caudal DRN, and a high proportion of galanin-positive cells in the midline also contained NADPH-d and neuronal NOS, thus suggesting a potential NO-galanin interaction in these neurons. The differential pattern of Fos/NADPH-d colocalization across the nucleus suggests that midline and lateral wing NOS neurons of the DRN express their neuromodulatory actions on discrete efferent targets via different intracellular mechanisms.
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PMID:Activity-dependent heterogeneous populations of nitric oxide synthase neurons in the rat dorsal raphe nucleus. 1661 32

1. Brief interruption of spinal cord blood flow resulting from transient abdominal aortic occlusion may lead to degeneration of specific spinal cord neurons and to irreversible loss of neurological function. The alteration of nitric oxide/nitric oxide synthase (NO/NOS) pool occurring after ischemic insult may play a protective or destructive role in neuronal survival of affected spinal cord segments. 2. In the present study, the spatiotemporal changes of NOS following transient ischemia were evaluated by investigating neuronal NOS immunoreactivity (nNOS-IR), reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry, and calcium-dependent NOS (cNOS) conversion of [(3)H] l-arginine to [(3)H] l-citrulline. 3. The greatest levels of these enzymes and activities were detected in the dorsal horn, which appeared to be most resistant to ischemia. In that area, the first significant increase in NADPHd staining and cNOS catalytic activity was found immediately after a 15-min ischemic insult. 4. Increases in the ventral horn were observed later (i.e., after a 24-h reperfusion period). While the most intense increase in nNOS-IR was detected in surviving motoneurons of animals with a shorter ischemic insult (13 min), the greatest increase of cNOS catalytic activity and NADPHd staining of the endothelial cells was found after stronger insult (15 min). 5. Given that the highest levels of nNOS, NADPHd, and cNOS were found in the ischemia-resistant dorsal horn, and nNOS-IR in surviving motoneurons, it is possible that NO production may play a neuroprotective role in ischemic/reperfusion injury.
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PMID:Spatiotemporal alterations of the NO/NOS neuronal pools following transient abdominal aorta occlusion: morphological and biochemical studies in the rabbit. 1678 31

The mesencephalic dorsolateral periaqueductal gray (dlPAG) mediates different modalities of aversive behaviors including pain and nociception and is anatomically delineated from other columns of the PAG by its content of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d). In many brain regions, neuronal NADPH-d is a nitric oxide (NO) synthase (NOS) and NO production mediates many nociceptive and aversive behavioral responses. The aim of this study was to determine how the noxious stimulant capsaicin affects intracellular dynamics in the dlPAG evidenced by Fos protein immunoreactivity (index of intracellular activation) and the NADPH-d reactivity. The basic hypothesis tested was that the effect of systemic capsaicin administration involved activation of the NO-producing machinery in the dlPAG. Compared to vehicle, capsaicin (50mg/kg, subcutaneous) significantly increased NADPH-d reactivity and Fos expression along the dlPAG neuraxis. However, less than one percent of the capsaicin-induced Fos activation occurred in NADPH-d-positive cells. This suggests that different intracellular mechanisms involving NO and activation of at least one other transmitter substance underlie the effects of capsaicin in the dlPAG. Although NADPH-d is a marker for constitutive NOS, only about two-thirds of the NADPH-d-positive neurons in the dlPAG were colocalized with neuronal NOS immunoreactive cells. This observation suggests that in contrast to other brain regions, neuronal NOS is unlikely to account for all NADPH-d activity in the dlPAG. Taken together, the present results show that the effect of capsaicin requires activation of at least one other transmitter and NADPH-d-dependent NO synthesis involving, but not limited to, the neuronal NOS isoform.
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PMID:Acute capsaicin injection increases nicotinamide adenine dinucleotide phosphate diaphorase staining independent of Fos activation in the rat dorsolateral periaqueductal gray. 1683 9

Nicotinamide Adenine Dinucleotide Phosphate-Diaphorase (NADPH-d) expressing neurons in the retina of golden hamsters have been identified to be a subset of amacrine cells that provide a major source of Nitric Oxide (NO) in retina. This subset of amacrine cells in mouse retina was recently proved to contain the circadian clock gene Per1 (D.Q. Zhang, T. Zhou, G.X. Ruan, D.G. McMahon, Circadian rhythm of Period 1 clock gene expression in NOS amacrine cells of the mouse retina, Brain Res., 1050 (2005) 101-109). However, it remains unknown whether these clock-related NADPH-d amacrine cells can be regulated by light stimulation and thus synchronized to ambient day/night cycle. A previous study has reported that NADPH-d expressing amacrine cells in postnatal hamsters exhibited a surge after eye-opening (D. Tay, Y.C. Diao, Y.M. Xiao, K.F. So, Postnatal development of nicotinamide adenine dinucleotide phosphate-diaphorase-positive neurons in the retina of the golden hamster, J. Comp. Neurol., 446 (2002) 342-348) suggesting a possible effect of light on the NADPH-d amacrine cells. In order to further reveal the relationship between NADPH-d amacrine cells and light stimulation, the present study focuses on the changes of the expression of NADPH-d in the retina of postnatal hamsters reared in completely deprived light conditions. Prior to eye opening, P12 hamster pups were subjected to either bilateral eyelid suturing or dark rearing. On P28 a subgroup of light deprived hamsters was returned to lighting conditions and the expression of NADPH-d activities in the retina was assessed. In hamsters reared in the 12:12 light-dark cycle, the number of NADPH-d amacrine cells in the ganglion cell layer (GCL) increased right after eye-opening and reached the adult level gradually. However, hamsters subjected to both bilateral eyelid suturing and dark rearing, the number of NADPH-d amacrine cells in GCL was maintained at a low level but increased again upon returning to the 12:12 light-dark condition. In contrast, the number of NADPH-d expressing amacrine cells in the inner nuclear layer (INL) remained low and unaltered regardless of the lighting environment. This study demonstrates that there are two subpopulations of NADPH-d expressing amacrine cells with respect to different locations in the retina of hamsters. Different from those in INL, the NADPH-d amacrine cells in GCL of postnatal hamsters are dependent on the lighting environment implicating that these clock-related amacrine cells and the production of NO might be under a modulation of light stimulation.
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PMID:Expression of nicotinamide adenine dinucleotide phosphate-diaphorase in the retina of postnatal golden hamsters deprived of light stimulation. 1685 23

After pelvic surgeries such as radical prostatectomy, two major complications--urinary incontinence and erectile dysfunction (ED) may occur. Etiologies for ED are multiple pathologic mediators/systems. Oxidative stress, which is known to be induced after surgical trauma, could be a cause of ED. The purposes of in this study are to investigate the effect of unilateral manipulation/ dissection and resection of the cavernous nerve (neurotomy) to NOS (nitric oxide synthase)-containing nerve fibers and pressure after electro stimulation in rat corpus cavernosum, and to determine whether these procedures would produce oxidative stress within rat cavernous tissue 3 weeks and 6 months after the operation. Male rats were divided into 5 groups. Rats in groups 1 and 2 underwent unilateral cavernous nerve manipulation and sacrificed 3 weeks and 6 months after the operation, respectively. Rats in groups 3 and 4 underwent unilateral neurotomy of a 5-mm. segment of the cavernous nerve, and they were sacrificed 3 weeks and 6 months after nerve ablation, respectively. Group 5 rats were control animals for biochemical analysis. Intracavernous pressure following electro stimulation reduced is significantly 3 weeks after unilateral resection, as compared to that of the manipulated nerve (P < 0.05), and it recovered 6 months after neurotomy. The recovery was also confirmed by NADPH (nicotinamide adenine dinucleotide phosphate) diaphorase staining in neurotomy groups. Lipid peroxidation, which is an indicater of oxidative stress, was determined by measuring thiobarbituric acid reacting substance (TBARS) levels and superoxide dismutase (SOD) activity. These markers indicated that unilateral cavernous nerve manipulation or resection produced oxidative stress within rat corpus cavernosum. Oxidative stress was more prominent 3 weeks after unilateral neurotomy (P < 0.05). Also, compared to the control animal group, oxidative stress was observed three weeks after manipulation of unilateral cavernous nerve (P < 0.05). Resection of the cavernous nerve caused more prominent oxidative stress than in the manipulation group. This study suggested, that unilateral cavernous neurotomy caused a decrease of intra cavernous pressure and NOS fibers in rat corpus cavernosum, and they recovered 6 months after neurotomy. Our data also provided evidence that neurotomy and manipulation of the cavernous nerve caused oxidative stress in rat corpus cavernosum and that oxidative stress was more prominent in the nerve resection group.
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PMID:Changes of nitric oxide synthase-containing nerve fibers and parameters for oxidative stress after unilateral cavernous nerve resection or manuplation in rat penis. 1697 Feb 48

The long-term benefits of nitroglycerin therapy are limited by tolerance development. Understanding the precise nature of mechanisms underlying nitroglycerin-induced endothelial cell dysfunction may provide new strategies to prevent tolerance development. In this line, we tested interventions to prevent endothelial dysfunction in the setting of nitrate tolerance. When bovine aortic endothelial cells (BAECs) were continuously treated with nitric oxide (NO) donors, including nitroglycerin, over 2-3 days, basal production of nitrite and nitrate (NO(x)) was diminished. The diminished basal NO(x) levels were mitigated by intermittent treatment allowing an 8-h daily nitrate-free interval during the 2- to 3-day treatment period. Addition of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor apocynin restored the basal levels of NO(x) that were decreased by continuous nitroglycerin treatment of BAECs. Apocynin caused significant improvement of increased mRNA and protein levels of endothelial nitric oxide synthase (eNOS) in BAECs given nitroglycerin continuously over the treatment period. Apocynin also reduced endothelial production of reactive oxygen species (ROS) after continuous nitroglycerin treatment. These results showed an essential similarity to the effects of a nitrate-free interval. Application of the NOS inhibitor N(omega)-nitro- l-arginine methyl ester caused a recovery effect on basal NO(x) and eNOS expression but was without effect on ROS levels in continuously NO donor-treated BAECs. In conclusion, the present study characterized abnormal features and functions of endothelial cells following continuous NO donor application. We suggest that inhibition of NADPH oxidase, by preventing NO donor-induced endothelial dysfunction, may represent a potential therapeutic strategy that confers protection from nitrate tolerance development.
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PMID:Possible usefulness of apocynin, an NADPH oxidase inhibitor, for nitrate tolerance: prevention of NO donor-induced endothelial cell abnormalities. 1744 45

It has been shown that the intrinsic mitochondrial apoptotic cascade is activated in vascular hyperpermeability after conditions such as hemorrhagic shock. Studies from our laboratory demonstrated mitochondrial reactive oxygen species (ROS) formation in endothelial cells during vascular hyperpermeability. We hypothesized that the participation of mitochondrial ROS in the intrinsic apoptotic cascade results in microvascular endothelial cell hyperpermeability. The purpose of this study was to identify the site(s) of ROS formation in the mitochondrial complex(es) that leads to hyperpermeability. Rat lung microvascular endothelial cell monolayers were pretreated with inhibitors of the complex(es) (I-V) before the activation of the mitochondrial apoptotic cascade using the proapoptotic peptide BAK (BH3). Inhibitors of the xanthine oxidase, nicotinamide adenine dinucleotide phosphate (reduced form) oxidase, NOS, and cytochrome P-450 monooxygenase were also studied. The hyperpermeability was determined by the fluorescence of fluorescein isothiocyanate-albumin that leaked across endothelial cells and ROS production by 2',7& rime;-dichlorofluorescein diacetate. Cytochrome c levels were also measured. BAK (BH3)-transfected cells showed increased ROS, cytosolic cytochrome c, and hyperpermeability (P<0.05). Complex III inhibitors antimycin A (10 microM) and stigmatellin (10 microM) attenuated BAK (BH3)-mediated ROS formation and hyperpermeability (P<0.05). The complex III inhibition decreased BAK (BH3)-mediated cytochrome c release. The results suggest that mitochondrial ROS formation, particularly at respiratory chain complex III, is involved in BAK-induced monolayer hyperpermeability.
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PMID:Mitochondrial complex III is involved in proapoptotic BAK-induced microvascular endothelial cell hyperpermeability. 1841 38


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