• Title/Summary/Keyword: Nitroprusside

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The effect of SKF S25A on SNP-, Ach-, or Pinacidil-Induced Relaxation in the Aorta of Rat (SKF 525A가 휜쥐의 대동맥에서 Sodium nitroprusside, Acetylcholine, Pinacidil에 의한 이완반응에 미치는 효과)

  • 박조영;김학림;김주원;신창열;최윤미;김진학;안형수;손의동;허인회
    • YAKHAK HOEJI
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    • v.44 no.1
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    • pp.80-86
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    • 2000
  • TEA, glibenclamide, L-NAME and SKF 525A-induced contraction were investigated using acetylcholine, sodium nitroprusside (SNP, NO donor) and pinacidil (ATP sensitive $K^{+}$ channel opener) in rat abdominal and thoracic aorta. The relaxant effects of acetylcholine, SNP and pinacidil were not different in the abdominal aorta and in the thoracic aorta. Acetylcholine-induced relaxation was dependent on endothelial cell, but pinacidil was independent endothelia cell. In the presence of TEA, glibenclamide, L-NAME, mepacrine and SKF 525A, acetylcholine and SNP did not change, but pinacidil-induced relaxation was significantly reduced in presence of glibenclamide, which is ATP sensitive $K^{+}$ channel blocker. SKF 525A, which is inhibitor of cytochrome P$_{450}$ dependent epoxygenase, partially inhibited the pinacidil-induced relaxation. These results indicate that the pinacidil-induced relaxation may be mediated by ATP sensitive $K^{+}$ channel and partially by EETs, which is produced by cytochrome P$_{450}$ dependent epoxygenase.enase.

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Inhibition of TCDD Induced Cyplal Expression by SNP In Hepa I Cells

  • Kim, Ji-E.;Sheen, Yhun-Y.
    • Biomolecules & Therapeutics
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    • v.7 no.4
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    • pp.315-321
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    • 1999
  • Since it has been known that hypoxia increases inducible nitric oxide synthase (iNOS) gene expression through hypoxia responsive element, it was possible to establish the hypothesis that nitric oxide could be a mediator of hypoxia to inhibit Cyplal promoter activity. In order to test this hypothesis, we have undertaken the study to examine the effects of hypoxia and nitric oxide on Cyplal promoter activity in Hepa I cells. Mouse Cyplal 5'flanking DNA, 1.6 Kb was cloned into pGL3 expression vector in order to construct pmCyplal-Luc. Hepa I cells were transfected with pmCyplal-Luc and were treated with $10^{-9}$ M TCDD and nitric oxide producing agents, such as lipopolysaccharide(LPS), sodium nitroprusside (SNP). Luciferase activity of reporter gene was measured from pmCyplal-Luc transfected Hepa I cell lysate which contains 2 g total protein using luciferin as a substrate. Nitric oxide producing agents, such as lipopolysaccharide (LPS), sodium nitroprusside(SNP) showed inhibition of luciferase activity that was induced by $10^{-9}$M TCDD treatment with dose dependent manner. Concomitant treatment of 1mM $N^G$-nitro-ι-arginine with $10^{-6}$~$10^{-4}$M sodium nitro-prusside recovered luciferase activity from the TCDD induced luciferase activity that was inhibited by nitric oxide producing agents. These demonstrated that nitric oxide could be a mediator of inhibitors on dioxin induced Cyplal expression in Hepa I cells.

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Resveratrol Inhibits Nitric Oxide-Induced Apoptosis via the NF-Kappa B Pathway in Rabbit Articular Chondrocytes

  • Eo, Seong-Hui;Cho, Hongsik;Kim, Song-Ja
    • Biomolecules & Therapeutics
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    • v.21 no.5
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    • pp.364-370
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    • 2013
  • Resveratrol (trans-3,4'-trihydroxystillbene), a naturally occurring polyphenolic antioxidant found in grapes and red wine, elicits diverse biochemical responses and demonstrates anti-aging, anti-inflammatory, and anti-proliferative effects in several cell types. Previously, resveratrol was shown to regulate differentiation and inflammation in rabbit articular chondrocytes, while the direct production of nitric oxide (NO) in these cells by treatment with the NO donor sodium nitroprusside (SNP) led to apoptosis. In this study, the effect of resveratrol on NO-induced apoptosis in rabbit articular chondrocytes was investigated. Resveratrol dramatically reduced NO-induced apoptosis in chondrocytes, as determined by phase-contrast microscopy, the MTT assay, FACS analysis, and DAPI staining. Treatment with resveratrol inhibited the SNP-induced expression of p53 and p21 and reduced the expression of procaspase-3 in chondrocytes, as detected by western blot analysis. SNP-induced degradation of I-kappa B alpha ($I{\kappa}B-{\alpha}$) was rescued by resveratrol treatment, and the SN50 peptide-mediated inhibition of NF-kappa B (NF-${\kappa}B$) activity potently blocked SNP-induced caspase-3 activation and apoptosis. Our results suggest that resveratrol inhibits NO-induced apoptosis through the NF-${\kappa}B$ pathway in articular chondrocytes.

Effects of Nitric Oxide on Inhibitory Receptors of Rod Bipolar Cells of Rat Retina

  • Park, No-Gi;Bai, Sun-Ho;Jung, Chang-sub;Chun, Mynng-Hoon
    • The Korean Journal of Physiology and Pharmacology
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    • v.9 no.6
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    • pp.347-352
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    • 2005
  • The effects of nitric oxide (NO) on inhibitory neurotransmitter receptors and some types of inhibitory receptors in dissociated rod bipolar cell (RBC) were investigated. In the whole cell voltage-clamping mode, the gamma-aminobutyric acid (GABA) activated current showed both sustained and transient components. GABA activated transient current was fully blocked by bicuculine, a $GABA_A$ receptor antagonist. The cis-4-aminocrotonic acid (CACA), a $GABA_C$ receptor agonist, evoked the sustained current that was not blocked by bicuculline (BIC). Glycine activated the transient current. These results indicate that the RBCs possess $GABA_A$, $GABA_C$, and glycine inhibitory receptors. Sodium nitroprusside (SNP), a NO analogue, reduced the currents activated by $GABA_A$ receptor only, however, did not reduce the currents activated by either $GABA_C$ or glycine receptors. This study signifies further that only NO depresses the fast inhibitory response activated by $GABA_A$ receptor in RBC. We, therefore, postulate that NO might depress the light-on/off transient inhibitory responses in RBCs in the rat retina.

The Role of Nitric Oxide in Menadione-Induced Cytotoxicity in Rat Platelets (Menadione에 의한 흰쥐 혈소판 세포독성에서 nitric oxide의 역할)

  • 승상애;김대병;윤여표;정진호
    • Toxicological Research
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    • v.11 no.2
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    • pp.303-308
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    • 1995
  • Nitric oxide, a physiological transmitter, is reported to mediate cellular injury in various tissues. Its reactivity to free radical is believed to be one of the reasons for its involvement in cytotoxicity. Menadione, a representative quinone, is cytotoxic to several cell systems including isolated hepatocyte, endothelial cell and red blood cells. Its toxic mechanism is related to oxidative stress, mediated by toxic free radicals. Our previous studies demonstrated that menadione induced cell lysis and increase of oxygen consumption in platelets. It has been reported that platelets have nitric oxide producing enzyme, nitric oxide synthase. Thus, we have investigated to manifest the role of nitric oxide.in menadione-induced cytotoxicity in rat platelets. Menadione induced cytotoxicity in platelets was unaffected by $N^G$-nitro-arginine methyl ester (L-NAME), selective and competitive inhibitor of nitric oxide synthase. We also invesitgated the role of extracellular nitric oxide in menadione-induced cytotoxicity of platelets by addition with sodium nitroprusside (SNP). SNP did not affect platelet cytotoxicity by menadione. These results suggested that nitric oxide which was generated endogeneously or exogeneously might have a negligible role in menadione-induced cytotoxicity in rat platelets.

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Sodium nitroprusside mediates seedling development and attenuation of oxidative stresses in Chinese cabbage

  • Sung, Chang-Hyun;Hong, Jeum-Kyu
    • Plant Biotechnology Reports
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    • v.4 no.4
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    • pp.243-251
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    • 2010
  • Nitric oxide (NO) has been shown to be involved in diverse physiological processes in microbes, animals and plants. In this study, the involvement of NO in the development and possible roles in oxidative stress protection of Chinese cabbage (Brassica rapa subsp. pekinensis cv. Samrack-ulgari) seedlings were investigated. Exogenous application of sodium nitroprusside (SNP) retarded root elongation, while increasing lateral root formation of Chinese cabbage. Plants showed no signs of external stress due to SNP application in true leaves. Cotyledons of 3-week-old Chinese cabbage plants were found to be highly sensitive to SNP application. Treated cotyledons displayed rapid tissue collapse and associated cell death. Although SNP application reduced root growth under normal growth conditions, it also enhanced methyl viologen (MV)-mediated oxidative stress tolerance. Analysis of SNP application to Chinese cabbage leaf disks, revealed SNP-induced tolerance against oxidative stresses by MV and $H_2O_2$, and evidence includes prevention of chlorophyll loss, superoxide anion (${O_2}^-$) accumulation and lipid peroxidation. This report supports a role for nitric oxide in modulating early seedling development, programmed cell death and stress tolerance in Chinese cabbage.

Protective Mechanism of Nitric Oxide and Mucus against Ischemia/Reperfusion-Induced Gastric Mucosal Injury

  • Kim, Hye-Young;Nam, Kwang-Soo;Kim, Kyung-Hwan
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.4
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    • pp.511-519
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    • 1998
  • This study investigated the role of nitric oxide on the oxidative damage in gastric mucosa of rats which received ischemia/reperfusion and its relation to mucus. Nitric oxide synthesis modulators such as L-arginine and $N^G-nitro-L-arginine$ methyl ester, and sodium nitroprusside, a nitric oxide donor, were injected intraperitoneally to the rats 30 min prior to ischemia/reperfusion which was induced by clamping the celiac artery and the superior mesenteric artery for 30 min and reperfusion for 1 h. Lipid peroxide production, the contents of glutathione and mucus, and glutathione peroxidase activities of gastric mucosa were determined. Histological observation of gastric mucosa was performed by using hematoxylin-eosin staining and scanning electron microscopy. The result showed that ischemia/reperfusion increased lipid peroxide production and decreased the contents of glutathione and mucus as well as glutathione peroxidase activities of gastric mucosa. Ischemia/reperfusion induced gastric erosion and gross epithelial disruption of gastric mucosa. Pretreatment of L-arginine, a substrate for nitric oxide synthase, and sodium nitroprusside prevented ischemia/reperfusion-induced alterations of gastric mucosa. However, $N^G-nitro-$ L- arginine methyl ester, a nitric oxide synthase inhibitor, deteriorated oxidative damage induced by ischemia/reperfusion. In conclusion, nitric oxide has an antioxidant defensive role on gastric mucosa by maintaining mucus, glutathione, and glutathione peroxidase of gastric mucosa.

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The Hyperthermic Effect of Nitric Oxide in Central Nervous System

  • Jung, Jae-Kyung;Sohn, Uy-Dong;Lee, Seok-Yong
    • The Korean Journal of Physiology and Pharmacology
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    • v.5 no.1
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    • pp.93-98
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    • 2001
  • The precise mechanism of set-point regulation in hypothalamus was not elucidated. Nitric oxide synthases(NOS) were detected in hypothalamus, however, the roles of NO in hypothalamus was not fully studied. So, we tested the effects of NO on body temperature because preoptic-anterior hypothalamus was known as the presumptive primary fever-producing site. NO donor sodium nitroprusside (SNP, 4 nmol, i.c.v.) elicited marked febrile response, and this febrile response was completely blocked by indomethacin (a cyclooxygenase inhibitor). But, ODQ (selective guanylate cyclase inhibitor, $50\;{\mu}g,$ i.c.v.) did not inhibit fever induced by SNP. The cyclic GMP analogue dibutyryl-cGMP $(100\;{\mu}g,\;i.c.v.)$ induced significant pyreses, which is blocked by indomethacin. $N^G-nitro-L-arginine$ methyl ester (L-NAME, non selective NOS inhibitor) inhibited fever induced by $interleukin-1{\beta}\;(IL-1{\bata},\;10\;ng,\;i.c.v.),$ one of endogenous pyrogens. These results indicate that NO may have an important role, not related to stimulation of soluble guanylate cyclase, in the signal pathway of thermoregulation in hypothalamus.

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Alleviating Effects of Nitric Oxide on Cadmium Toxicity in White Poplar (Populus alba)

  • Semsettin Kulac;Yakup Cikili;Halil Samet;Ertugrul Filiz
    • Journal of Forest and Environmental Science
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    • v.40 no.1
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    • pp.43-52
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    • 2024
  • Cadmium (Cd) is non-essential heavy metal that negatively affects plant metabolism. Nitric oxide (NO) is an increasingly important molecule for plant metabolism that makes signaling. In this study, it was aimed to investigate the alleviating effect of sodium nitroprusside (SNP) application as NO donor in white poplar (Populus alba) under Cd stress conditions. SNP and without SNP treatments increased the Cd accumulation in root tissue. While photosynthetic pigments (Chl a, Chl b, Chl a+b, and carotenoid) content decreased by only Cd application, SNP+Cd application decreased the rate of photosynthetic pigments reduction. When the results of Cd and Cd+SNP applications were evaluated for mineral (Fe, Zn, Mn and Cu) uptake, it was found that the positive effect of SNP was heterogeneously affected. Depending on SNP application, it was found that malondialdehyde (MDA) amount decreased in leaf in 100 µM Cd applications while hydrogen peroxide (H2O2) amount decreased in 100 and 500 µM Cd applications. When antioxidant enzyme activities were examined, it was found that catalase (CAT) and ascorbate peroxidase (APX) enzyme activities increased with 100 µM SNP applications under all Cd applications. As a result, it was found that SNP application under Cd stress generally supports physiological processes positively in white poplar, suggesting that NO molecule plays important alleviating roles in plant metabolism.

The Effect of Nitric Oxide, Isosorbide Dinitrate and Sodium Nitroprusside on Ischemic Myocardium of Rat (Nitric oxide, Isosorbide dinitrate 및 Sodium nitroprusside가 쥐의 허혈성 심근에 미치는 영향)

  • Jeong, Jong-Hwa;Kim, Su-Hyeon;Kim, Song-Myeong
    • Journal of Chest Surgery
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    • v.29 no.10
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    • pp.1055-1065
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    • 1996
  • This experiment was undertaken to assess the effect of nitric oxide, isosorbide dinitrate, and sodium nitroprusside, which are known to increase coronary flow by vasodilation and to improve the cardiac function of an ischemic heart The experiment was carried out to investigate the effect of nitric oxide on the coronary artery of an ischemic rat myocardium using isolated constant pressure Langendorfr system. The experimental parameters were lactate and CK-MB for the frozen myocardium and coronary flow. the quantity of coyonary flow, left ventricular developed pressure (LVDP), and dp/dt. The experimental groups were decided as control group (Group I), nitric oxide group (Group II), Iso orbide dinitrate group (Group III) and sodium nitroprusside group (Group IV). Statistical analysis was performed using repeated measured analysis of variance and 2tudent t-test The results were as follows: 1 . The lactic acid contents of group II and IV were less than other groups for the frozen myocardium at preischemic state (p< 0.0025), whereas the determined coronary flows were higher. 2. In the ratio of produced lactic acid between the preischemia and reperfusion for the coronary flow, group II and IV exhibitrod less value than others (p< 0.005). 3. Group II and III were less than others in the coronary flow for the quantity of CK-MB, but or the frozen myocardium, group II and IV were less. 4. Group II and IV showed higher coronary flow compared to others throughout entire experimental period (p< 0.005). 5. Group II was highest at the preischemic state for the left ventricular developed pressure. 6. The +maximal dp/dt of group II was highest compared to others. 7. Group I exhibi ed the highest recovery rate of coronary flow between prelschemla and reperfusion. 8. The(-dp/dt)1(+dp/dt) ratio was 116%, 100%, 100%, and 55% for the 4 groups, respectively And the recovery rate of total dp/dt was 34%, 67%, 51%, and 76% for the four groups, respectively.

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