l arginine/hypoxia

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Acute hypoxia increases intracellular L-arginine content in cultured porcine pulmonary artery endothelial cells.

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Exposure to hypoxia (0% O2) for 4-24 h resulted in increased intracellular L-arginine content and increased activity of calpain, a calcium-dependent neutral cysteine protease, in pulmonary artery endothelial cells. Calpain-inhibitor I abolished the increased L-arginine content in hypoxic cells. When

NG-nitro-L-arginine protects against hypoxia/hypoglycemia-induced decrease in CA1 presynaptic spikes in rat hippocampal slices.

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The effects of nitric oxide (NO) synthase inhibitors on the hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes elicited by stimulation of the Schaffer collaterals were investigated using rat hippocampal slices. Drugs were added to normal medium for 10 min before incubation under

L-arginine prevents hypoxia-induced vasoconstriction in dual-perfused human placental cotyledons.

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BACKGROUND Chronic hypoxia in the uteroplacental unit is associated with increased resistance to blood flow in the fetal-placental circulation. These changes can lead to adverse cardiovascular events in adulthood. This study investigates whether L-arginine (substrate for nitric oxide synthase (NOS)

Effects of L-arginine and L-carnitine in hypoxia/reoxygenation-induced intestinal injury.

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BACKGROUND This study was designed to show the role of oxidative stress, nitric oxide and glutathione-related antioxidant enzymes in hypoxia/reoxygenation (H/R)-induced intestinal injury model in mice and to evaluate the potential benefits of arginine and carnitine supplementation. METHODS A total

[The effects of long-term application of L-arginine on K+ channel in pulmonary artery smooth muscle cells from rats exposed to chronic hypoxia].

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OBJECTIVE To investigate the effects of long-term application of L-arginine (L-Arg) on K(+) channel in pulmonary artery smooth muscle cells (PASMC) from rats exposed to chronic hypoxia. METHODS Male Wistar rats were randomly divided into three groups: group A (control group), group B (chronic

The evaluation of hypoxia-inducible factor 1 in N-nitro-L-arginine methyl ester preeclampsia model of pregnant rats.

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OBJECTIVE The objective of the study was to evaluate hypoxia-inducible factor 1 (HIF-1), which plays a major role in the stimulation of angiogenesis in placental tissues, by using immunohistochemical staining in preeclampsia model of rats, developed by N-nitro-L-arginine methyl ester (L-NAME)

Nitric oxide pros and cons: The role of L-arginine, a nitric oxide precursor, and idebenone, a coenzyme-Q analogue in ameliorating cerebral hypoxia in rat.

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Evidence exists that nitric oxide (NO) may mediate both protective and pathological responses during brain hypoxia (HP). Reactive oxygen species have also been implicated in the pathophysiological response of the brain tissues to HP. Therefore, this study investigated whether a NO precursor,

Nomega-Nitro-L-Arginine Benzyl Ester Enhances Pulmonary Vasopressor Responses to Hypoxia and to Angiotensin II.

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The effects of Nomega-nitro-L-arginine benzyl ester (L-NABE), an inhibitor of nitric oxide (NO) synthase, were investigated on pulmonary arterial responses during baseline or low tone conditions and during elevated tone conditions induced by ventilatory hypoxia or by AII in the isolated

Induction of hypoxia in experimental murine tumors by the nitric oxide synthase inhibitor, NG-nitro-L-arginine.

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The nitric oxide synthase inhibitor NG-nitro-L-arginine (NOARG) was examined for its ability to alter energy metabolism in three murine tumors using 31P magnetic resonance spectroscopy. NOARG (10 mg/kg, i.v.) increased the inorganic phosphate:total phosphate ratio (Pi:total) 2-3-fold in the KHT,

Carnosine and L-arginine attenuate the downregulation of brain monoamines and gamma aminobutyric acid; reverse apoptosis and upregulate the expression of angiogenic factors in a model of hemic hypoxia in rats.

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The purpose of the present study was to investigate the preventive effect of L-arginine (ARG) and carnosine (CAR) on hypoxia-induced neurotoxicity in rats. The impact on neuro-inflammation, apoptosis, angiogenesis, and the brain levels of monoamines and GABA were

[Intermittent hypoxic training and L-arginine as corrective agents for myocardial energy supply under acute hypoxia].

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It NO has been shown play to the primary role in several mitochondrial functions. Our aim for this study was to investigate whether exogenous NO (L-arginine) or NO blocker L-NNA modulated the adaptive reactions of rat myocardial tissue respiration on intermittent hypoxic training (IHT). In the

Effect of maternal NG-nitro-l-arginine administration on fetal growth and hypoxia-induced changes in newborn rats.

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BACKGROUND Nitric oxide (NO) inhibition with NG-nitro-l-arginine methyl ester (l-NAME) in the last trimester of pregnancy caused intrauterine growth retardation and hind-limb disruptions in rats. In the present study, the effect of maternal NO inhibition with NG-nitro-l-arginine (l-NNA) on hypoxic

Inhibition of hypoxia-induced relaxation of rabbit isolated coronary arteries by NG-monomethyl-L-arginine but not glibenclamide.

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1. The effects of NG-monomethyl-L-arginine, tetrodotoxin and glibenclamide on hypoxia-induced coronary artery relaxation, induced by bubbling Krebs solution with 95% N2 and 5% CO2 instead of 95% O2 and 5% CO2, were assessed by measuring the changes in isometric tension in isolated epicardial

[Exogenous L-arginine modulates mitochondrial and microsomal oxidation in acute and intermittent normobaric hypoxia].

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It is known that protective effects of adaptation to intermittent hypoxia are mediated partly by stimulating of some mitochondrial and microsomal enzymes activity. Our objective was to investigate whether exogenous NO (L-arginine) or NO blocker (L-NNA) modulate mitochondrial and microsomal oxidation

Chronic renal hypoxia after acute ischemic injury: effects of L-arginine on hypoxia and secondary damage.

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Ischemic acute renal failure (ARF) results in the permanent loss of peritubular capillaries and predisposes the progression of chronic renal failure. The present study was undertaken to determine whether renal hypoxia, which may represent an important mediator in disease progression, is persistently

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