Effect of nitric oxide on the respiratory activity generated under hypoxic conditions by medullo-spinal preparations from early postnatal rats

1997 ◽  
Vol 29 (6) ◽  
pp. 334-342
Author(s):  
D. V. Volgin ◽  
V. A. Marchenko ◽  
M. M. Seredenko
Keyword(s):  
Nitric Oxide ◽  
Respiratory Activity ◽  
Hypoxic Conditions ◽  
Postnatal Rats

Differences in nitric oxide production: a comparison of retinal ganglion cells and retinal glial cells cultured under hypoxic conditions

2003 ◽  
Vol 112 (1-2) ◽  
pp. 126-134 ◽  
Author(s):  
Kenji Kashiwagi ◽  
Yoko Iizuka ◽  
Seiichi Mochizuki ◽  
Yuichi Tsumamoto ◽  
Hiromu K Mishima ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Retinal Ganglion Cells ◽  
Glial Cells ◽  
Ganglion Cells ◽  
Nitric Oxide Production ◽  
Retinal Ganglion ◽  
Oxide Production ◽  
Hypoxic Conditions ◽  
Cells Cultured

Nitric oxide inhibits HIF-1α protein accumulation under hypoxic conditions: implication of 2-oxoglutarate and iron

Biochimie ◽  
2006 ◽  
Vol 88 (5) ◽  
pp. 411-418 ◽  
Author(s):  
Anna V. Kozhukhar ◽  
Inna M. Yasinska ◽  
Vadim V. Sumbayev
Keyword(s):  
Nitric Oxide ◽  
Protein Accumulation ◽  
Hypoxic Conditions

scholarly journals Ferric Uptake Regulator-Dependent Antinitrosative Defenses in Salmonella enterica Serovar Typhimurium Pathogenesis

2013 ◽  
Vol 82 (1) ◽  
pp. 333-340 ◽  
Author(s):  
Maroof Husain ◽  
Jessica Jones-Carson ◽  
Lin Liu ◽  
Miryoung Song ◽  
J. Royden Saah ◽  
...  
Keyword(s):  
Iron Homeostasis ◽  
Nitrosative Stress ◽  
Respiratory Activity ◽  
Aminolevulinic Acid ◽  
Critical Role ◽  
Systemic Infection ◽  
Ferric Uptake Regulator ◽  
Content Type ◽  
Hypoxic Conditions ◽  
Serovar Typhimurium

ABSTRACTHerein we report an important role for the ferric uptake regulator (Fur) in the resistance ofSalmonellaentericaserovar Typhimurium to the reactive nitrogen species produced by inducible nitric oxide (NO) synthase in an NRAMP1rmurine model of acute systemic infection. The expression offurprotectedSalmonellagrown under normoxic and hypoxic conditions against the bacteriostatic activity of NO. The hypersusceptibility offur-deficientSalmonellato the cytotoxic actions of NO coincides with a marked repression of respiratory activity and the reduced ability of the bacteria to detoxify NO. AfurmutantSalmonellastrain contained reduced levels of the terminal quinol oxidases of the electron transport chain. Addition of the heme precursor δ-aminolevulinic acid restored the cytochrome content, respiratory activity, NO consumption, and wild-type growth in bacteria undergoing nitrosative stress. The innate antinitrosative defenses regulated by Fur added to the adaptive response associated with the NO-detoxifying activity of the flavohemoprotein Hmp. Our investigations indicate that, in addition to playing a critical role in iron homeostasis, Fur is an important antinitrosative determinant ofSalmonellapathogenesis.

scholarly journals Bacillus anthracis co-opts nitric oxide and host serum albumin for pathogenicity in hypoxic conditions

2013 ◽  
Vol 3 ◽  
Author(s):  
Stephen St. John ◽  
Ryan Blower ◽  
Taissia G. Popova ◽  
Aarthi Narayanan ◽  
Myung-Chul Chung ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Serum Albumin ◽  
Bacillus Anthracis ◽  
Hypoxic Conditions

Xanthine oxidoreductase catalyses the reduction of nitrates and nitrite to nitric oxide under hypoxic conditions

FEBS Letters ◽  
1998 ◽  
Vol 427 (2) ◽  
pp. 225-228 ◽  
Author(s):  
Timothy M Millar ◽  
Cliff R Stevens ◽  
Nigel Benjamin ◽  
Robert Eisenthal ◽  
Roger Harrison ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Xanthine Oxidoreductase ◽  
Hypoxic Conditions

Alternative oxidase is an important player in the regulation of nitric oxide levels under normoxic and hypoxic conditions in plants

2019 ◽  
Vol 70 (17) ◽  
pp. 4345-4354 ◽  
Author(s):  
Aprajita Kumari ◽  
Pradeep Kumar Pathak ◽  
Mallesham Bulle ◽  
Abir U Igamberdiev ◽  
Kapuganti Jagadis Gupta
Keyword(s):  
Nitric Oxide ◽  
Alternative Oxidase ◽  
Plant Mitochondria ◽  
No Production ◽  
Complex Iv ◽  
Increase Energy Efficiency ◽  
Hypoxic Conditions ◽  
Cytochrome Pathway ◽  
Important Player ◽  
Elicitor Treatments

Abstract Plant mitochondria possess two different pathways for electron transport from ubiquinol: the cytochrome pathway and the alternative oxidase (AOX) pathway. The AOX pathway plays an important role in stress tolerance and is induced by various metabolites and signals. Previously, several lines of evidence indicated that the AOX pathway prevents overproduction of superoxide and other reactive oxygen species. More recent evidence suggests that AOX also plays a role in regulation of nitric oxide (NO) production and signalling. The AOX pathway is induced under low phosphate, hypoxia, pathogen infections, and elicitor treatments. The induction of AOX under aerobic conditions in response to various stresses can reduce electron transfer through complexes III and IV and thus prevents the leakage of electrons to nitrite and the subsequent accumulation of NO. Excess NO under various stresses can inhibit complex IV; thus, the AOX pathway minimizes nitrite-dependent NO synthesis that would arise from enhanced electron leakage in the cytochrome pathway. By preventing NO generation, AOX can reduce peroxynitrite formation and tyrosine nitration. In contrast to its function under normoxia, AOX has a specific role under hypoxia, where AOX can facilitate nitrite-dependent NO production. This reaction drives the phytoglobin–NO cycle to increase energy efficiency under hypoxia.

scholarly journals Nitric oxide-mediated vasodilation becomes independent of β-adrenergic receptor activation with increased intensity of hypoxic exercise

2011 ◽  
Vol 110 (3) ◽  
pp. 687-694 ◽  
Author(s):  
Darren P. Casey ◽  
Timothy B. Curry ◽  
Brad W. Wilkins ◽  
Michael J. Joyner
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Brachial Artery ◽  
Exercise Intensity ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Adrenergic Mechanisms ◽  
Hypoxic Conditions ◽  
Forearm Exercise ◽  
Hypoxic Exercise

Hypoxic vasodilation in skeletal muscle at rest is known to include β-adrenergic receptor-stimulated nitric oxide (NO) release. We previously reported that the augmented skeletal muscle vasodilation during mild hypoxic forearm exercise includes β-adrenergic mechanisms. However, it is unclear whether a β-adrenergic receptor-stimulated NO component exists during hypoxic exercise. We hypothesized that NO-mediated vasodilation becomes independent of β-adrenergic receptor activation with increased exercise intensity during hypoxic exercise. Ten subjects (7 men, 3 women; 23 ± 1 yr) breathed hypoxic gas to titrate arterial O2 saturation to 80% while remaining normocapnic. Subjects performed two consecutive bouts of incremental rhythmic forearm exercise (10% and 20% of maximum) with local administration (via a brachial artery catheter) of propranolol (β-adrenergic receptor inhibition) alone and with the combination of propranolol and nitric oxide synthase inhibition [ NG-monomethyl-l-arginine (l-NMMA)] under normoxic and hypoxic conditions. Forearm blood flow (FBF, ml/min; Doppler ultrasound) and blood pressure [mean arterial pressure (MAP), mmHg; brachial artery catheter] were assessed, and forearm vascular conductance (FVC, ml·min−1·100 mmHg−1) was calculated (FBF/MAP). During propranolol alone, the rise in FVC (Δ from normoxic baseline) due to hypoxic exercise was 217 ± 29 and 415 ± 41 ml·min−1·100 mmHg−1 (10% and 20% of maximum, respectively). Combined propranolol-l-NMMA infusion during hypoxic exercise attenuated ΔFVC at 20% (352 ± 44 ml·min−1·100 mmHg−1; P < 0.001) but not at 10% (202 ± 28 ml·min−1·100 mmHg−1; P = 0.08) of maximum compared with propranolol alone. These data, when integrated with earlier findings, demonstrate that NO contributes to the compensatory vasodilation during mild and moderate hypoxic exercise; a β-adrenergic receptor-stimulated NO component exists during low-intensity hypoxic exercise. However, the source of the NO becomes less dependent on β-adrenergic mechanisms as exercise intensity increases.

Increased endothelin-1 and endothelin receptor expression in myocytes of ischemic and reperfused rat hearts and ventricular myocytes exposed to ischemic conditions and its inhibition by nitric oxide generation

2003 ◽  
Vol 81 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Xiaohong Tracey Gan ◽  
Subrata Chakrabarti ◽  
Morris Karmazyn
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Ventricular Myocytes ◽  
Receptor Expression ◽  
Neonatal Rat ◽  
No Donor ◽  
Myocardial Ischemia And Reperfusion ◽  
Endothelin 1 ◽  
Hypoxic Conditions ◽  
Rat Hearts

Endothelin-1 (ET-1) and nitric oxide (NO) exert opposite effects in the cardiovascular system, and there is evidence that the NO counters the potential deleterious effects of ET-1. We investigated whether NO affects the increased mRNA expression of ET-1 and endothelin receptors induced by (i) 30 min of ischemia with or without 30 min reperfusion in myocytes from isolated rat hearts or (ii) ischemic conditions (acidosis or hypoxia) in cultured rat neonatal ventricular myocytes. Ischemia with or without reperfusion produced more than a twofold increase in mRNA expression of ET-1 as well as the ETAand ETBreceptor (P < 0.05), although these effects were completely blocked by the NO donor 3-morpholinosydnonimine (SIN-1; 1 μM). To assess the possible factors regulating ET expression, myocytes were exposed to acidosis (pH 6.8–6.2) or to hypoxic conditions in an anaerobic chamber for 24 h in the presence or absence of SIN-1. At all acidic pHs, ET-1 and ETAreceptor mRNA expression was significantly (P < 0.05) elevated approximately threefold, although the magnitude of elevation was independent of the degree of acidosis. These effects were completely prevented by SIN-1. ETBreceptor expression was unaffected by acidosis. Hypoxia increased ET-1 as well as ETAand ETBreceptor expression threefold (P < 0.05), although this was unaffected by SIN-1. Our results demonstrate that myocardial ischemia and reperfusion upregulate the ET system, which is inhibited by NO. Although increased expression of the ET system can be mimicked by both acidosis and hypoxia, only the effects of the former are NO sensitive. NO may serve an endogenous inhibitory factor which regulates the expression of the ET system under pathological conditions.Key words: ET-1, ET receptors, NO, neonatal rat ventricular myocytes, hypoxia, acidosis.

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