Nitric oxide

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Nitric oxide-donor SNAP induces Xenopus eggs activation.

Nitric oxide-donor SNAP induces Xenopus eggs activation.

expressed and located near nucleus in Xenopus oocytes. Therefore, the role of RYR is rather considered as modest for endogenous calcium release mechanisms in contrast to pig oocytes [69,70]. Our results suggest that nitric oxide specifically induces parthe- nogenetic activation in Xenopus laevis eggs, through a calcium dependent mechanism, though the origin of the calcium changes in our context remains to be determined. Cell cycle control and progression, such as maturation and activation processes, imply different ionic modifications, including particularly calcium [71]. Calcium sources could be differently mobilized and result in dramatic as well as discrete changes, at local levels. For example, it is well known that, in mature oocyte, IP3 receptors are clustering at the membrane of the endoplasmic reticulum [72,73]. This could be responsible for calcium variations in restricted areas – microdomains - where calcium concentration could rise but may be also difficult to detect and measure by oocyte imaging.
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Nitric oxide synthase and polycystic kidney disease

Nitric oxide synthase and polycystic kidney disease

The -786 C allele of promoter polymorphism acts as a repressor of NOS3 transcription (12). The Glu298Asp and intron-4 VNTR are also known to alter endothelial NOS expression (11,13). Various studies have shown that nitric oxide synthase gene polymorphisms in PKD. A re- cent report on “nitric oxide synthase VNTR (intron 4 a/b) polymorphism and PKD” is very interesting (14). Eluma- lai et al studied the clinical relationship between VNTR genetic polymorphism and clinical course in patients with ADPKD (14). Elumalai et al showed the “significant as- sociation between the 27-bp VNTR and chronic kidney disease (CKD) advancement among the ADPKD patients in the South Indian population (14). The other study by analyzing four tagging SNPs and two more well studied polymorphisms (Intron 4 VNTR and Glu298Asp) of the NOS3 gene investigated to identify the potential modifier effect of NOS3 gene on the progression of CKD in AD- PKD (15). However, they did not find any evidence for the involvement of NOS3 tag-SNPs in the progression to CKD in ADPKD patients (15). Direct analysis of NOS3 gene polymorphisms in ADPKD patients has also revealed in- conclusive results from many populations (Table 1). Multiple studies have shown that nitric oxide negative- ly regulates the renin-angiotensin aldosterone system (RAAS) by inhibiting ACE activity and angiotensin II type 1 receptors (27). Use of angiotensin converting en- zyme inhibitors (ACE inhibitors) and angiotensin recep- tor blockers (ARBs) in controlling the CKD progression is further supporting the role of endothelial nitric oxide synthase.
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Nitric oxide transport in normal human thoracic aorta: effects of hemodynamics and nitric oxide scavengers.

Nitric oxide transport in normal human thoracic aorta: effects of hemodynamics and nitric oxide scavengers.

Nitric oxide (NO) secreted by vascular endothelium is a pivotal regulator in vascular homeostasis, and the change in its bioavailability has been proposed as a major mechanism of endothelial dysfunction and a crucial modulator of vascular diseases such as atherosclerosis and arterial aneurysm [1,2]. The hallmark of endothelial dysfunction is the impaired shear stress- dependent vasodilation mediated by NO [1]. In addition to causing smooth muscle relaxation, endothelial NO possesses many cardiovascular protective functions [3]. It can reduce endothelial permeability and thus suppress the influx of lipoproteins into the vascular wall. Besides, NO can also inhibit the oxidation of low density lipoproteins, prevent leukocytes from adhesion to the endothelium and hence migration into the vascular wall, and inhibit the proliferation/migration of vascular smooth muscle cells. Moreover, NO may inhibit platelet aggregation and adhesion to the vascular walls, hence preventing thrombosis.
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Setting reference values for exhaled nitric oxide

Setting reference values for exhaled nitric oxide

This is the first systematic review concerning reference values for exhaled nitric oxide. Fifteen studies met the selection criteria, and the factors and statistical models used to derive reference equations were retrieved. We have observed great variation in the factors and statis- tical methods used, which prevents an adequate com- parison of reference values from different studies. With current published data, the selection of reference equa- tions for FeNO is a difficult task for laboratories and physicians.

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Nitric oxide as a regulator of inflammatory processes

Nitric oxide as a regulator of inflammatory processes

Alfred Nobel’s pioneering work on the manufacture and use of nitroglycerin as an explosive culminated in his discovery of dynamite. In medicine, nitroglycerin is known more as the prototypical nitrosovasodilator, still widely used for treatment of angina, than for its explosive properties. Just over a hundred years after his death, the Nobel Prize in Physiology/Medicine was presented to Drs Robert Furchgott, Ferid Murad, and Louis Ignarro, in part for their demonstration that nitric oxide (NO) was the molecule generated from nitroglycerin that mediated its vasodilatory effects. This activity of NO had been previ- ously termed “endothelial-derived relaxing factor”.
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Genetic responses against nitric oxide toxicity

Genetic responses against nitric oxide toxicity

The threat of free radical damage is opposed by coordinated responses that modulate expression of sets of gene products. In mammalian cells, 12 proteins are induced by exposure to nitric oxide (NO) levels that are sub-toxic but exceed the level needed to activate guanylate cyclase. Heme oxygenase 1 (HO-1) synthesis increases substantially, due to a 30- to 70-fold increase in the level of HO-1 mRNA. HO-1 induction is cGMP-independent and occurs mainly through increased mRNA stability, which therefore indicates a new NO-signaling pathway. HO-1 induction contributes to dramatically increased NO resistance and, together with the other inducible functions, constitutes an adap- tive resistance pathway that also defends against oxidants such as H 2 O 2 . In E. coli, an oxidative stress response, the soxRS regulon, is
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Signaling in the nitric oxide system

Signaling in the nitric oxide system

nitric oxide synthase (NOS) enzymes. All cytosolic NOS isoforms have L-arginine and oxygen as substrates and NADPH as an electron donor to form NO, thus leading to the production of NO, citrulline and water (26). Three cytosolic NOS isoforms have been identified so far. Two of them are constitutively expressed and are calcium-de- pendent, and their nomenclature was created based on the cells in which they are predominating found: the neu- ronal isoform (nNOS, or type 1, NOS-1), and the endothe- lial isoform (eNOS, or type 3, NOS-3). The inducible isoform (iNOS, or type II, NOS-2) is calcium-independent and its expression was found to be inducible in different tissues. Indeed, it was found that neurons can also express eNOS and that iNOS expression can be induced in neuronal cultures by cytokines. Astrocytes can also express eNOS and, when activated by inflammatory mediators, may ex- press iNOS (27).
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Alendronate induces gastric damage by reducing nitric oxide synthase expression and NOcGMPKATP signaling pathway

Alendronate induces gastric damage by reducing nitric oxide synthase expression and NOcGMPKATP signaling pathway

Takeuchi, Role of nitric oxide in regulation of gastric acid secretion in rats: effects of NO donors and NO synthase inhibitor, Br. Kim, Effects of a nitric oxide donor and nitric oxide [r]

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The role of nitric oxide in reproduction

The role of nitric oxide in reproduction

Nitric oxide (NO) plays a crucial role in reproduction at every level in the organism. In the brain, it activates the release of luteinizing hormone-releasing hormone (LHRH). The axons of the LHRH neu- rons project to the mating centers in the brain stem and by afferent pathways evoke the lordosis reflex in female rats. In males, there is activation of NOergic terminals that release NO in the corpora cavernosa penis to induce erection by generation of cyclic guanosine monophos- phate (cGMP). NO also activates the release of LHRH which reaches the pituitary and activates the release of gonadotropins by activating neural NO synthase (nNOS) in the pituitary gland. In the gonad, NO plays an important role in inducing ovulation and in causing luteolysis, whereas in the reproductive tract, it relaxes uterine muscle via cGMP and constricts it via prostaglandins (PG).
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Novel donors of nitric oxide derived of

Novel donors of nitric oxide derived of

The nitric oxide (NO) radical is an impor- tant and versatile mediator in biological sys- tems (1). This molecule is known to play an important role in the regulation of a wide range of physiological processes. NO is bio- synthesized from L-arginine by NO synthases (NOS) in a two-step oxidation process (2) and has an extremely short lifetime. In order to increase its stability to reach its biological targets, NO radical must be carried by chem- ical species. It has been suggested that NO radical is stabilized in vivo by reactions with molecules such as proteins containing nu- cleophilic residues or bioinorganic molecules (3,4).
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Application of a nitric oxide sensor in biomedicine

Application of a nitric oxide sensor in biomedicine

were designed for in vivo and large surfaces (cultured cells), works with the inNO-T meter with easy calibration procedures. The inNO-Tcombine both a NO configured potentiostat and a software controlled data acquisition system included in one battery powered unit. The ―amiNO‖ series sensor is covered with a triplecoat gas permeable membrane to guarantee selectivity and fast response time. The NO diffuses through the membrane and is then oxidized at the working platinum electrode, resulting in an electric current. The redox current is proportional to the NO concentration outside the membrane and is continuously monitorized with an inNO-TM software (version 1.9 supplied by Innovative Instruments Inc.) installed on a PC computer. The calibration curve and its representative appear in Figure 1 of our published previous work [16]. Briefly, the sensor is calibrated by a simple, economical, and a reliable chemical reaction for NO production. This reaction is based on the conversion of nitrite to nitric oxide in acidic solution in the presence of iodide ion. The reaction has a ratio of one to one, meaning that the amount of NO produced in this reaction equal to the amount of nitrite added.
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Targeting and translocation of endothelial nitric oxide synthase

Targeting and translocation of endothelial nitric oxide synthase

In different tissues and for different NOS isoforms, NO synthesis has been identified within a variety of subcellular organelles (reviewed in Ref. 7). In contrast to the other NOS isoforms, the targeting of eNOS to the particulate subcellular fraction was observed in the initial characterizations of the purified enzyme, which documented that detergents are required for eNOS solubilization (8). When molecular clones for eNOS were iden- tified, it was noted that eNOS contains no hydrophobic transmembrane domain, and it was subsequently established that the asso- ciation of eNOS with cell membranes is mediated principally by enzyme acylation (reviewed in Ref. 9). Nitric oxide is a labile molecule, and may play important biological roles both within the cell in which it is synthesized and in its interactions with nearby cells and molecules (10,11). NO may be either stabilized or degraded through its in- teractions with diverse intracellular or extra- cellular chemical moieties. The localization of NOS within the cell might therefore be expected to influence the biological role and chemical fate of the NO produced by the enzyme.
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Nitric oxide paradox in asthma

Nitric oxide paradox in asthma

Role of lipopolysaccharides (LPS), nitric oxide synthase 2 (NOS2) and arginase 1 (Arg1) in airway inflammation. Upon inhalation of allergen (OVA) and LPS, two metabolic pathway are activated, Arg1 and NOS2, respectively. The Arg1 pathway is triggered by type 2 cytokines (IL-4, IL-10, IL-13) released from OVA-specific Th2 effector cells. Concomitantly, LPS signaling via toll-like receptor 4 (TLR4) activates NOS2 isoform. The Arg1 pathway is down regulated by L-hidroxy arginine (L-OH arginine) a product of NOS2 pathway whereas the NOS2 pathway is down modulated by consumption of L-arginine and by polyamines that are end products of Arg1 pathway. Consequently, low concentrations of NO are produced which favor peroxynitrite (ONOO - ) formation. NO at low concentrations and
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New nitric oxide donors based on ruthenium complexes

New nitric oxide donors based on ruthenium complexes

49. Rodrigues GJ, Lunardi CN, Lima RG, Santos CX, Laurindo FR, da Silva RS, et al. Vitamin C improves the effect of a new nitric oxide donor on the vascular smooth muscle from renal hypertensive rats. Nitric Oxide 2008; 18: 176-183. 50. Oliveira-Sales EB, Dugaich AP, Carillo BA, Abreu NP, Boim

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Nitric oxide synthesis and biological functions of nitric oxide released from ruthenium compounds

Nitric oxide synthesis and biological functions of nitric oxide released from ruthenium compounds

During three decades, an enormous number of studies have demonstrated the critical role of nitric oxide (NO) as a second messenger engaged in the activation of many systems including vascular smooth muscle relaxation. The underlying cellular mechanisms involved in vasodilatation are essentially due to soluble guanylyl-cyclase (sGC) modulation in the cytoplasm of vascular smooth cells. sGC activation culminates in cyclic GMP (cGMP) production, which in turn leads to protein kinase G (PKG) activation. NO binds to the sGC heme moiety, thereby activating this enzyme. Activation of the NO-sGC-cGMP-PKG pathway entails Ca 2+ signaling reduction and vasodilatation. Endothelium dysfunction leads to decreased production or bioavailability of endogenous NO that could contribute to vascular diseases. Nitrosyl ruthenium complexes have been studied as a new class of NO donors with potential therapeutic use in order to supply the NO deficiency. In this context, this article shall provide a brief review of the effects exerted by the NO that is enzymatically produced via endothelial NO-synthase (eNOS) activation and by the NO released from NO donor compounds in the vascular smooth muscle cells on both conduit and resistance arteries, as well as veins. In addition, the involvement of the nitrite molecule as an endogenous NO reservoir engaged in vasodilatation will be described.
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Cellular signaling with nitric oxide and cyclic GMP

Cellular signaling with nitric oxide and cyclic GMP

ronments (see 7 and references therein). A rapidly advancing area of clinical ap- plication is the inhalation of low concentra- tions of the NO gas (see 7 and references therein). Inhalation of low concentrations of NO has been beneficial in infants, children and adults with pulmonary hypertension, bronchospasm, and right to left cardiac shunts from congenital heart defects. Interestingly, nitric oxide at low concentrations is quite stable and minimally reactive. However, at higher concentrations NO can interact with many transition metals, heme-containing pro- teins, and thiol groups and can oxidize functionalities on polynucleotides (RNA and DNA) and proteins and can form strand breaks in polynucleotides (Figure 6).
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Characterization of Nitric Oxide Reductase (NOR) from Pseudomonas nautica, a Study on Biologic Nitric Oxide Reduction

Characterization of Nitric Oxide Reductase (NOR) from Pseudomonas nautica, a Study on Biologic Nitric Oxide Reduction

The Nitric oxide reductases (NOR) catalyze the third step in the denitrification pathway. Protein sequence alignment with members from this classe can be checked in the supporting information S1. They are divided in three different classes, according to their physiological electron donor: the cytochromes (cNOR), quinol (qNOR) and the copper quinol (qCuNOR) [7] (figure 1.5). These enzymes are integral membrane proteins, and they belong to the heme copper oxidase (HCuO) superfamily, sharing a high structural homology of the catalytic subunit. In this class of enzymes, there is variation in the type of electron transfer co-factors and in the number of subunits, but very well conserved is the unusual binuclear diiron center, composed by a b-type heme (heme b 3 )
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Inhaled nitric oxide and high concentrations of oxygen in pediatrics patients with congenital cardiopathy and pulmonary hypertension: report of five cases

Inhaled nitric oxide and high concentrations of oxygen in pediatrics patients with congenital cardiopathy and pulmonary hypertension: report of five cases

w orsening of hypoxem ia and overload of the right ventricle. T hese cardiopathies lead to hypertrophy and hyperplasia of the vascular m usculature and consequent vasoconstriction. C onventional treatm ent after, surgery consists of using hyperventilation, alkalization, increase in the inhaled oxygen fraction, inotropics and vasodilators. T he great advantage in using inhaled nitric oxide (N O ) is that, contrary to system ic vasodilators, it only reaches the ventilated alveoli, thereby causing selective pulm onary vasodilation (2,3) w ith deviation of the flow

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Neuronal and endothelial nitric oxide synthase gene knockout mice

Neuronal and endothelial nitric oxide synthase gene knockout mice

Targeted disruption of the neuronal nitric oxide synthase (nNOS) and endothelial nitric oxide synthase (eNOS) genes has led to knockout mice that lack these isoforms. These animal models have been useful to study the roles of nitric oxide (NO) in physiologic processes. nNOS knockout mice have enlarged stomachs and defects in the inhibitory junction potential involved in gastrointestinal motility. eNOS knock- out mice are hypertensive and lack endothelium-derived relaxing factor activity. When these animals are subjected to models of focal ischemia, the nNOS mutant mice develop smaller infarcts, consistent with a role for nNOS in neurotoxicity following cerebral ischemia. In contrast, eNOS mutant mice develop larger infarcts, and show a more pronounced hemodynamic effect of vascular occlusion. The knockout mice also show that nNOS and eNOS isoforms differentially modulate the release of neurotransmitters in various regions of the brain. eNOS knockout mice respond to vessel injury with greater neointimal prolif- eration, confirming that reduced NO levels seen in endothelial dys- function change the vessel response to injury. Furthermore, eNOS mutant mice still show a protective effect of female gender, indicating that the mechanism of this protection cannot be limited to upregula- tion of eNOS expression. The eNOS mutant mice also prove that eNOS modulates the cardiac contractile response to ß-adrenergic agonists and baseline diastolic relaxation. Atrial natriuretic peptide, upregulated in the hearts of eNOS mutant mice, normalizes cGMP levels and restores normal diastolic relaxation.
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Nitric oxide decomposition on copper supported on zeolites.

Nitric oxide decomposition on copper supported on zeolites.

NITRIC OXIDE DECOMPOSITION ON COPPER SUPPORTED ON ZEOLITES. Direct decomposition of NO on copper supported on zeolite catalysts such as MCM-22 and Beta was compared with that on the thoroughly studied Cu-ZSM-5. The catalysts were prepared by ion-exchange in basic media. They were characterized by atomic absorption, surface area, nitrogen adsorption at 77K, X-ray diffraction and temperature programmed reduction. The products of the reaction were analyzed by Fourier transform infrared spectroscopy using a gas cell. Catalytic activity tests indicated that zeolite catalysts, like Beta and MCM-22, lead to NO conversion values comparable to ZSM-5.
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