Practical nitric oxide measurement employing a nitric oxide-selective electrode

Ichimori, Kohji; Ishida, Hideyuki; Fukahori, Masami; Nakazawa, Hiroe; Murakami, Eiichi

doi:10.1063/1.1144674

Cited by 176 publications

(114 citation statements)

References 15 publications

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“…Tip diameter of the probe (25 m) permitted the use of a micromanipulator (ZeissEppendorff) attached to the stage of an inverted microscope (Nikon Diaphot) and enclosed in a Faraday's chamber to position the sensor approximately 5 m above the cell surface. Calibration of the electrochemical sensor was performed using different concentrations of a nitrosothiol NO donor S-nitroso-N-acetyl-DL-penicillamine, as previously detailed (23).…”

Section: Methodsmentioning

confidence: 99%

Permissive Role of Nitric Oxide in Endothelin-induced Migration of Endothelial Cells

Noiri

Bahou

et al. 1997

Journal of Biological Chemistry

152

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Endothelin (ET) synthesis is enhanced at sites of ischemia or in injured vessels. The purpose of this study was to explore the possibility of autocrine stimulation of endothelial cell migration by members of the endothelin family. Experiments with microvascular endothelial cell transmigration in a Boyden chemotactic apparatus showed that endothelins 1 and 3, as well as a selective agonist of ET B receptor IRL-1620, equipotently stimulated migration. Endothelial cell migration was unaffected by the blockade of ET A receptor, but it was inhibited by ET B receptor antagonism. Based on our previous demonstration of signaling from the occupied ET B receptor to constitutive nitric oxide (NO) synthase (Tsukahara, H., Ende, H., Magazine, H. I., Bahou, W. Formation of new blood vessels, driven by the morphogenetic program and/or by the functional demand for increased blood supply, is initiated by the budding of endothelial cells off the microcirculatory bed. Tissue hypoxia represents a physiologic stimulus for angiogenesis, and several autocrine angiogenic mediators produced by endothelial cells have been recognized (1-3). Endothelin, one of such mediators, is constitutively produced by endothelial cells and its production is enhanced by hypoxia (4 -6). Two investigative teams have recently demonstrated that ET-1 1 and ET-3, acting via the ET B receptor, stimulate endothelial cell migration and proliferation (7, 8).Since we and others have previously demonstrated that occupancy of ET B receptors in endothelial cells is accompanied by the activation of constitutive endothelial NO synthase (9, 10), we hypothesized that the observed motogenic effects of members of the ET family may in fact be mediated by the release of NO. Indeed, there is emerging evidence that NO release serves as a prerequisite for epithelial and endothelial cell motility (11-13). Leibovich et al. (13) have shown that production of angiogenic activity by activated monocytes (assayed by chemotaxis of endothelial cells and corneal angiogenesis) is absolutely dependent on L-arginine and NO synthase. These observations are in concert with findings reported by Ziche et al. (12) who detected the potentiation by sodium nitroprusside of the angiogenic effect of substance P in the rabbit cornea. Our own observations expand this function to the classical angiogenic signal, vascular endothelial growth factor. We demonstrated that endogenous NO production by the endothelial cells is a prerequisite for the motogenic and angiogenic effects of this factor.2 In the present study, we used three different approaches (migration and wound healing by endothelial cells, wound healing by Chinese hamster ovary cells expressing ET B receptor with or without eNOS, and application of antisense oligodeoxynucleotides targeting eNOS) to provide evidence that the effect of ET-1 on cell migration is mediated via ET B receptor and requires functional enzymatic machinery for NO generation. MATERIALS AND METHODSCell Culture and Reagents-Renal microvascular endothelial cells (RMVEC) were...

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Section: Methodsmentioning

confidence: 99%

Permissive Role of Nitric Oxide in Endothelin-induced Migration of Endothelial Cells

Noiri

Bahou

et al. 1997

Journal of Biological Chemistry

152

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“…The current increased linearly from 1.5 to 305 pA when the S-nitroso-N-acetyl-dl-penicillamine (SNAP) concentration increased from 5 nmol/L to 1 mol/L. 39 We measured ACh (1 mol/L)-stimulated NO release in ring segments from rabbit aortas (3 mm wide) cut longitudinally and mounted on a silicone plate in the Krebs-Henseleit tissue bath that was saturated with 95% O 2 /5% CO 2 . With the use of a micropositioner (0.2-mm x-y-z resolution), the microsensor was placed at a 0.2-mm distance from the surface of endothelial cells in the aorta.…”

Section: Measurement Of No By An No Electrodementioning

confidence: 99%

Dehydroepiandrosterone Retards Atherosclerosis Formation Through Its Conversion to Estrogen

Hayashi

Esaki

Muto

et al. 2000

ATVB

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Abstract-Dehydroepiandrosterone (DHEA) is speculated to have an antiatherosclerotic effect, although the mechanism of action remains unclear. The objective of the current study was to determine whether the antiatherosclerotic effect of DHEA is related to its conversion to estrogen and to define the role of nitric oxide (NO) in the antiatherosclerotic effect of DHEA. Forty-eight oophorectomized rabbits were divided into 5 groups and fed the following diets for 10 weeks: group 1, a regular rabbit diet plus 1% cholesterol (a high-cholesterol diet [HCD]); group 2, an HCD plus 0.3% DHEA; group 3, an HCD plus 0.3% DHEA and fadrozole (2.0 mg ⅐ kg Ϫ1 ⅐ d Ϫ1 ), a specific aromatase inhibitor; group 4, an HCD plus 17␤-estradiol (20 g ⅐ kg Ϫ1 ⅐ d Ϫ1 ); and group 5, a regular diet. Atherosclerotic lesions, lipid deposition in aortic vessels, and basal and stimulated NO release were measured in the aforementioned groups of rabbits. NO release was measured by using an NO-selective electrode as well as by measuring vascular responses and the plasma NO metabolites nitrite and nitrate. The plasma total cholesterol level was increased, but there were no significant differences in lipid profile in the 4 groups of rabbits that were fed the HCD. The area occupied by atherosclerosis in the thoracic aorta was diminished by Ϸ60% in the DHEA-treated rabbits (group 2) compared with the HCD group of rabbits (group 1); there was a corresponding 80% decrease in the estradiol group (group 4) but only a 30% decrease in the DHEA plus fadrozole group (group 3). In the aortas of rabbits from groups 1 and 3, the acetylcholine-induced and tone-related basal NO-mediated relaxations were diminished compared with those of the controls (group 5). However, these relaxations were restored in the aortas of group 2 and 4 rabbits, and an increase in NO release was observed in groups 2 and 4 compared with groups 1 and 3, as measured by an NO-selective electrode. Injection of neither solvent (20% ethanol/distilled water) nor fadrozole significantly affected the atherosclerotic area or the NO-related responses described above. We conclude that Ϸ50% of the total antiatherosclerotic effect of DHEA was achieved through the conversion of DHEA to estrogen. NO may also play a role in the antiatherosclerotic effect of DHEA and 17␤-estradiol. have not yet been determined. In plasma, where the major portion of these hormones is present in the sulfate form, it is possible that DHEA-S serves as a reservoir for DHEA, since various tissues have been shown to contain steroid sulfatases. 1 The peak plasma levels of DHEA and DHEA-S occur at approximately age 25 years, decrease progressively thereafter, and diminish by 95% around the age of 85 years. Epidemiological evidence has shown that adult men with high plasma DHEA-S levels are less likely to die of cardiovascular disease. 2 A study indicated that administration of DHEA reduced aortic fatty streak formation and cholesterol accumulation by Ϸ30% to 40% in cholesterol-fed rabbits. 3 Another report has shown a 50% reduction...

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“…Cu(I), releases NO. This method of NO calibration is generally accepted as being suitable for most NO sensors [25][26][27][28][29]. However, SNAP does have drawbacks relating to its stability and purity, because it is extremely sensitive to light and temperature [21,25,30,31].…”

Section: Introductionmentioning

confidence: 99%

Calibration of NO sensors for in-vivo voltammetry: laboratory synthesis of NO and the use of UV?visible spectroscopy for determining stock concentrations

et al. 2005

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The increasing scientific interest in nitric oxide (NO) necessitates the development of novel and simple methods of synthesising NO on a laboratory scale. In this study we have refined and developed a method of NO synthesis, using the neutral Griess reagent, which is inexpensive, simple to perform, and provides a reliable method of generating NO gas for in-vivo sensor calibration. The concentration of the generated NO stock solution was determined using UV-visible spectroscopy to be 0.28±0.01 mmol L À1 . The level of NO 2 À contaminant, also determined using spectroscopy, was found to be 0.67±0.21 mmol L À1 . However, this is not sufficient to cause any considerable increase in oxidation current when the NO stock solution is used for electrochemical sensor calibration over physiologically relevant concentrations; the NO sensitivity of bare Pt-disk electrodes operating at +900 mV (vs. SCE) was 1.08 nA lmol À1 L, while that for NO 2 À was 5.9·10 À3 nA lmol À1 L. The stability of the NO stock solution was also monitored for up to 2 h after synthesis and 30 min was found to be the time limit within which calibrations should be performed.

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Practical nitric oxide measurement employing a nitric oxide-selective electrode

Cited by 176 publications

References 15 publications

Permissive Role of Nitric Oxide in Endothelin-induced Migration of Endothelial Cells

Permissive Role of Nitric Oxide in Endothelin-induced Migration of Endothelial Cells

Dehydroepiandrosterone Retards Atherosclerosis Formation Through Its Conversion to Estrogen

Calibration of NO sensors for in-vivo voltammetry: laboratory synthesis of NO and the use of UV?visible spectroscopy for determining stock concentrations

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