l arginine/hypoxia

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

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

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)

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

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

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)

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,

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

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,

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

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

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

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

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