Respiratory alkalosis does not alter NOx  concentrations in human plasma and erythrocytes

Ishibashi, Takaharu; Kubota, Kaname; Himeno, Mariko; Matsubara, Taku; Hori, Tomoyuki; Ozaki, Kazuyuki; Yamozoe, Masaru; Aizawa, Yoshifusa; Yoshida, Junko; Nishio, Matomo

doi:10.1152/ajpheart.2001.281.6.h2757

Cited by 17 publications

(22 citation statements)

References 14 publications

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“…Indeed, experiments that examined the effectiveness of DIDS had been performed in blood-free systems, but to our knowledge, there are no data on inertness in protein-rich (or biological) fluid. Therefore, it would be worth calling attention to the inertness in such circumstances to avoid wrong interpretation of results obtained from inappropriate experimental conditions (4).…”

Section: Effect Of Dids On No3mentioning

confidence: 99%

“…Among these factors, the possible accumulation of NO 3 -into erythrocytes (RBCs) through anion exchanger (AE1) has received attention as a modulating mechanism of plasma NO 3 -(almost all NOx in plasma) concentration (3), although the operation of this mechanism seems to be unlikely in healthy subjects (4). Recently, Herken et al (5) reported higher NOx concentrations in washed RBCs of patients with schizophrenia, compared with control subjects.…”

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confidence: 99%

“…All experiments were performed at 37°C. NOx concentrations in plasma, PBS, and in hemolysate were determined by HPLC-Griess system (Eicom, Kyoto); and NOx concentration in RBC was calculated as described previously (4). Although NO 2 -and NO 3 -were separately determined, the amount of NO 2 -was quite small and the relative values of the two ions were not accurate in the hemolysate.…”

mentioning

confidence: 99%

“…Although NO 2 -and NO 3 -were separately determined, the amount of NO 2 -was quite small and the relative values of the two ions were not accurate in the hemolysate. Thus, the measured values were expressed as NOx (sum of two ions) (4). Pure water [resistance >18.3 MW and virtually NOx-free through MILLI-Q SP (Millipore, Bedford, MA, USA)] was used for the preparation of all solutions described in this study, and all laboratory ware was washed five times with pure water to minimize NOx contamination (7).…”

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confidence: 99%

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Effects of 4,4'-Diisothiocyanato-stilbene-2,2'-disulfonic Acid (DIDS) and Chlorpromazine on NO3− Transport via Anion Exchanger in Erythrocytes: Inertness of DIDS in Whole Blood

et al. 2003

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Abstract. We examined the effects of chlorpromazine on NO 3 -transport between erythrocytes (RBCs) and extracellular fluid. Chlorpromazine (10 m g / ml) did not influence NO 3 -movement in both whole blood and RBC suspension. Though an anion exchanger (AE1) inhibitor DIDS (4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid, 100 mM) did not alter NO 3 -movement in whole blood, it inhibited the movement in a concentration-dependent manner in the RBC suspension. The inhibition was abrogated by plasma and albumin concentration-dependently. Our results indicated that chlorpromazine had no effect on NO 3 -transport through AE1 and that the inertness of DIDS on AE1 in whole blood is due to interference by albumin in plasma. ) concentration has been used as an index of NO formation in vivo in spite of the high susceptibility to many confounding factors (1, 2). Among these factors, the possible accumulation of NO 3 -into erythrocytes (RBCs) through anion exchanger (AE1) has received attention as a modulating mechanism of plasma NO 3 -(almost all NOx in plasma) concentration (3), although the operation of this mechanism seems to be unlikely in healthy subjects (4). Recently, Herken et al. (5) reported higher NOx concentrations in washed RBCs of patients with schizophrenia, compared with control subjects. This result was inconsistent with our experience that the washing procedure could partially or completely reduce RBC NOx to a level equivalent to that in the washing solution. Therefore, it is difficult to accept the argument advanced by Herken et al. (5) that higher NOx concentration in the blood (hence in RBCs) reflects increment of NO formation in schizophrenia. However, a possible interpretation remains for the discrepancy. Since their patients were treated with neuroleptics (5), including chlorpromazine and haloperidol (6), it is possible that these agents may prevent NO 3 -transport through AE1. To test this hypothesis, we examined whether these agents could modify NO 3 -transport across the RBC cell membrane via AE1. In a previous study (4), we could not confirm the contribution of AE1 to NO 3 -transport in whole blood using 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS), an AE1 inhibitor. Accordingly, experiments were performed using both whole blood and RBC suspension. We also examined the cause of inertness of DIDS in whole blood.Venous blood samples were drawn from healthy volunteers of both sexes (28 -50-year-old) after obtaining written consent. The study was approved by the Human Ethics Committee of Kanazawa Medical University. The blood sample was immediately heparinized and used directly or as RBC suspension. Phosphatebuffered saline (PBS; 10 mM, pH 7.4, NOx <0.1 m M) was prepared and RBCs were washed with five volumes of the buffer followed by centrifugation. The buffy coat

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Section: Effect Of Dids On No3mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Effects of 4,4'-Diisothiocyanato-stilbene-2,2'-disulfonic Acid (DIDS) and Chlorpromazine on NO3− Transport via Anion Exchanger in Erythrocytes: Inertness of DIDS in Whole Blood

et al. 2003

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“…After centrifugation (10000ϫg for 10 min at 4°C), the supernatant was directly used for NO x determination as described elsewhere. 22) We determined NO x levels using an HPLC-Griess system (ENO10 and ENO20; Eicom, Kyoto, Japan) consisting of a separation column, a flow reactor (with Griess reagent), a reduction column, and a detector at 540 nm, as described elsewhere. 13) Operating under default conditions, the detection limit and sensitivity was 0.1 mM for both NO 2 Ϫ and NO 3 Ϫ with a loading volume of 10 ml.…”

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Different Disappearance Rates of Plasma Nitrite (NO2-) Contribute to Apparent Steady-State Arterio-Venous Differences in Anesthetized Animals

Ishibashi

Nishizawa

Nakamoto-Nomura

et al. 2011

Biological & Pharmaceutical Bulletin

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) is not only an oxidative product of nitric oxide (NO), but also serves as an indicator of endothelial nitric oxide synthase activity and as a circulating reservoir of NO bioactivity in the circulatory system. [1][2][3] The indicator status is supported by observations that approximately 70-90% of circulating plasma NO 2 Ϫ levels derive from NO produced by endothelial nitric oxide synthase. 4,5) The reservoir activity is widely accepted (see reviews [1][2][3] ) as is maintained when NO 2 Ϫ reacts with deoxygenated hemoglobin (Hb) in red blood cells (RBCs) to form NO and methemoglobin (metHb), leading to biological responses including vasodilation.2,6,7) Therefore, precise evaluation of NO 2 Ϫ plasma levels, including detailed kinetic knowledge, is required for further understanding of NO 2 Ϫ biology in the circulation. However, only limited kinetic data [8][9][10] are presently available, and many problems of NO 2 Ϫ biology await resolution.For example, it is still controversial whether arterio-venous (A-V) differences in plasma NO 2 Ϫ levels actually exist. 10-16)The A-V difference may reflect consumption of NO 2 Ϫ to form NO during peripheral circulation for preservation of blood flow at lower oxygen tension.12) Although we have previously reported a small but significant A-V difference under steadystate conditions, 10,14,17) these observations are complicated by a report that, in isolated blood, uptake of NO 2 Ϫ by RBCs is faster in venous blood than in arterial blood, 15) a scenario that may cause artificial apparent A-V differences when arterial and venous blood samples are treated after some delay. If this situation is indeed the case, our previous work reporting kinetic parameters 10) should also be re-evaluated. It is also unclear whether plasma NO 2 Ϫ levels reflect in vivo changes in NO 2 Ϫ levels. 10,12,18) Exogenously administered NO 2 Ϫ or NO resulted in a large A-V difference in plasma NO 2 Ϫ , with arterial blood preferentially reflecting the changes, 10,14,17) presumably due to greater contributions by RBCs or tissue as a buffering compartment under a state of lower oxygenation. A possible difference in the uptake rate of RBCs could not be large enough to explain such a large A-V difference, and contributions of tissue factors would be a great concern. 18,19) The emerging role of tissue as a reservoir of NO bioactivity via NO 2 Ϫ should be taken into consideration; some reports indicate that plasma NO 2 Ϫ levels may not accurately reflect increases in NO or NO 2 Ϫ levels in biological systems. 3,20,21) However, no alternative measures exist for assessing NO bioactivity in easily accessible biomaterials (such as blood). Therefore, the aim of this study was to estimate the steady-state concentration of plasma NO 2 Ϫ in order to evaluate whether the putative A-V difference actually exists. We also re-evaluated the pertinent kinetic features in vivo, considering uptake by RBC and tissue factors. MATERIALS AND METHODSJapanese white rabbits weighing 2.4-3.5 kg were anesthetized with intravenous sodium...

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Association between coronary endothelial dysfunction and local inflammation of atherosclerotic coronary arteries

Matsubara

Ishibashi

Hori³

et al. 2003

Biochemistry of Diabetes and Atherosclerosis

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Respiratory alkalosis does not alter NOx concentrations in human plasma and erythrocytes

Cited by 17 publications

References 14 publications

Effects of 4,4'-Diisothiocyanato-stilbene-2,2'-disulfonic Acid (DIDS) and Chlorpromazine on NO3− Transport via Anion Exchanger in Erythrocytes: Inertness of DIDS in Whole Blood

Effects of 4,4'-Diisothiocyanato-stilbene-2,2'-disulfonic Acid (DIDS) and Chlorpromazine on NO3− Transport via Anion Exchanger in Erythrocytes: Inertness of DIDS in Whole Blood

Different Disappearance Rates of Plasma Nitrite (NO2-) Contribute to Apparent Steady-State Arterio-Venous Differences in Anesthetized Animals

Association between coronary endothelial dysfunction and local inflammation of atherosclerotic coronary arteries

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