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Jon O Lundberg – One of the best experts on this subject based on the ideXlab platform.

  • nadph oxidase in the renal microvasculature is a primary target for blood pressure lowering effects by inorganic nitrate and Nitrite
    Hypertension, 2015
    Co-Authors: Ting Yang, Jon O Lundberg, Eddie Weitzberg, Maria Peleli, Christa Zollbrecht, Erik A G Persson, Mattias Carlstrom

    Renal oxidative stress and nitric oxide (NO) deficiency are key events in hypertension. Stimulation of a nitrateNitrite–NO pathway with dietary nitrate reduces blood pressure, but the mechanisms or target organ are not clear. We investigated the hypothesis that inorganic nitrate and Nitrite attenuate reactivity of renal microcirculation and blood pressure responses to angiotensin II (ANG II) by modulating nicotinamide adenadenineudinucleotide phosphate (NADPH) oxidase activity and NO bioavailability. Nitrite in the physiological range (10 −7 –10 −5 mol/L) dilated isolated perfused renal afferent arterioles, which were associated with increased NO. Contractions to ANG II (34%) and simultaneous NO synthase inhibition (56%) were attenuated by Nitrite (18% and 26%). In a model of oxidative stress (superoxide dismutase-1 knockouts), abnormal ANG II–mediated arteriolar contractions (90%) were normalized by Nitrite (44%). Mechanistically, effects of Nitrite were abolished by NO scavenger and xanthine oxidase inhibitor, but only partially attenuated by inhibiting soluble guanylyl cyclase. Inhibition of NADPH oxidase with apocynin attenuated ANG II–induced contractility (35%) similar to that of Nitrite. In the presence of Nitrite, no further effect of apocynin was observed, suggesting NADPH oxidase as a possible target. In preglomerular vascular smooth muscle cells and kidney cortex, Nitrite reduced both basal and ANG II–induced NADPH oxidase activity. These effects of Nitrite were also abolished by xanthine oxidase inhibition. Moreover, supplementation with dietary nitrate (10 −2 mol/L) reduced renal NADPH oxidase activity and attenuated ANG II–mediated arteriolar contractions and hypertension (99±2–146±2 mm Hg) compared with placebo (100±3–168±3 mm Hg). In conclusion, these novel findings position NADPH oxidase in the renal microvasculature as a prime target for blood pressure–lowering effects of inorganic nitrate and Nitrite.

  • physiological role for nitrate reducing oral bacteria in blood pressure control
    Free Radical Biology and Medicine, 2013
    Co-Authors: Vikas Kapil, Jon O Lundberg, Eddie Weitzberg, Vanessa Pearl, Syed M A Haydar, Amrita Ahluwalia

    Circulating nitrate (NO3−), derived from dietary sources or endogenous nitric oxide production, is extracted from blood by the salivary glands, accumulates in saliva, and is then reduced to Nitrite (NO2−) by the oral microflora. This process has historically been viewed as harmful, because Nitrite can promote formation of potentially carcinogenic N-nitrosamines. More recent research, however, suggests that Nitrite can also serve as a precursor for systemic generation of vasodilatory nitric oxide, and exogenous administration of nitrate reduces blood pressure in humans. However, whether oral nitrate-reducing bacteria participate in “setting” blood pressure is unknown. We investigated whether suppression of the oral microflora affects systemic Nitrite levels and hence blood pressure in healthy individuals. We measured blood pressure (clinic, home, and 24-h ambulatory) in 19 healthy volunteers during an initial 7-day control period followed by a 7-day treatment period with a chlorhexidine-based antiseptic mouthwash. Oral nitrate-reducing capacity and Nitrite levels were measured after each study period. Antiseptic mouthwash treatment reduced oral Nitrite production by 90% (p < 0.001) and plasma Nitrite levels by 25% (p = 0.001) compared to the control period. Systolic and diastolic blood pressure increased by 2–3 .5 mm Hg, increases correlated to a decrease in circulating Nitrite concentrations (r2 = 0.56, p = 0.002). The blood pressure effect appeared within 1 day of disruption of the oral microflora and was sustained during the 7-day mouthwash intervention. These results suggest that the recycling of endogenous nitrate by oral bacteria plays an important role in determination of plasma Nitrite levels and thereby in the physiological control of blood pressure.

  • Nitrate and Nitrite in biology, nutrition and therapeutics
    Nature Chemical Biology, 2009
    Co-Authors: Jon O Lundberg, Nathan S Bryan, Mark T Gladwin, Nigel Benjamin, Amrita Ahluwalia, Anthony Butler, Pedro Cabrales, Angela Fago, Martin Feelisch, Peter C Ford

    Inorganic nitrate and Nitrite from endogenous or dietary sources are metabolized in vivo to nitric oxide (NO) and other bioactive nitrogen oxides. The nitrateNitrite-NO pathway is emerging as an important mediator of blood flow regulation, cell signaling, energetics and tissue responses to hypoxia. The latest advances in our understanding of the biochemistry, physiology and therapeutics of nitrate, Nitrite and NO were discussed during a recent 2-day meeting at the Nobel Forum, Karolinska Institutet in Stockholm.

Zoltan Mester – One of the best experts on this subject based on the ideXlab platform.

Jose E Tanussantos – One of the best experts on this subject based on the ideXlab platform.

  • gastric s nitrosothiol formation drives the antihypertensive effects of oral sodium Nitrite and nitrate in a rat model of renovascular hypertension
    Free Radical Biology and Medicine, 2015
    Co-Authors: Lucas C Pinheiro, Jefferson H Amaral, Graziele C Ferreira, Rafael L Portella, Carla S Ceron, Marcelo F Montenegro, Jose Carlos Toledo, Jose E Tanussantos

    Many effects of Nitrite and nitrate are attributed to increased circulating concentrations of Nitrite, ultimately converted into nitric oxide (NO•) in the circulation or in tissues by mechanisms associated with Nitrite reductase activity. However, Nitrite generates NO• , nitrous anhydride, and other nitrosating species at low pH, and these reactions promote S-nitrosothiol formation when Nitrites are in the stomach. We hypothesized that the antihypertensive effects of orally administered Nitrite or nitrate involve the formation of S-nitrosothiols, and that those effects depend on gastric pH. The chronic effects of oral Nitrite or nitrate were studied in two-kidney, one-clip (2K1C) hypertensive rats treated with omeprazole (or vehicle). Oral Nitrite lowered blood pressure and increased plasma S-nitrosothiol concentrations independently of circulating Nitrite levels. Increasing gastric pH with omeprazole did not affect the increases in plasma Nitrite and nitrate levels found after treatment with Nitrite. However, treatment with omeprazole severely attenuated the increases in plasma S-nitrosothiol concentrations and completely blunted the antihypertensive effects of Nitrite. Confirming these findings, very similar results were found with oral nitrate. To further confirm the role of gastric S-nitrosothiol formation, we studied the effects of oral Nitrite in hypertensive rats treated with the glutathione synthase inhibitor buthionine sulfoximine (BSO) to induce partial thiol depletion. BSO treatment attenuated the increases in S-nitrosothiol concentrations and antihypertensive effects of oral Nitrite. These data show that gastric S-nitrosothiol formation drives the antihypertensive effects of oral Nitrite or nitrate and has major implications, particularly to patients taking proton pump inhibitors.

  • tempol enhances the antihypertensive effects of sodium Nitrite by mechanisms facilitating Nitrite derived gastric nitric oxide formation
    Free Radical Biology and Medicine, 2013
    Co-Authors: Jefferson H Amaral, Lucas C Pinheiro, Graziele C Ferreira, Marcelo F Montenegro, Rafael P Barroso, Antonio J Costafilho, Jose E Tanussantos

    Abstract Orally administered Nitrite exerts antihypertensive effects associated with increased gastric nitric oxide (NO) formation. While reducing agents facilitate NO formation from Nitrite, no previous study has examined whether antioxidants with reducing properties improve the antihypertensive responses to orally administered Nitrite. We hypothesized that TEMPOL (4-hydroxy-2,2,6,6-tetramethylpiperidine-N-oxyl) could enhance the hypotensive effects of Nitrite in hypertensive rats by exerting antioxidant effects (and enhancing NO bioavailability) and by promoting gastric Nitrite-derived NO generation. The hypotensive effects of intravenous and oral sodium Nitrite were assessed in unanesthetized freely moving rats with L-NAME (Nω-nitro- L- arginine methyl ester; 100 mg/kg; po)-induced hypertension treated with TEMPOL (18 mg/kg; po) or vehicle. While TEMPOL exerted antioxidant effects in hypertensive rats, as revealed by lower plasma 8-isoprostane and vascular reactive oxygen species levels, this antioxidant did not affect the hypotensive responses to intravenous Nitrite. Conversely, TEMPOL enhanced the dose-dependent hypotensive responses to orally administered Nitrite, and this effect was associated with higher increases in plasma Nitrite and lower increases in plasma nitrate concentrations. In vitro experiments using electrochemical and chemiluminescence NO detection under variable pH conditions showed that TEMPOL enhanced Nitrite-derived NO formation, especially at low pH (2.0 to 4.0). TEMPOL signal evaluated by electron paramagnetic resoresonance decreased when Nitrite was reduced to NO under acidic conditions. Consistent with these findings, increasing gastric pH with omeprazole (30 mg/kg; po) attenuated the hypotensive responses to Nitrite and blunted the enhancement in plasma Nitrite concentrations and hypotensive effects induced by TEMPOL. Nitrite-derived NO formation in vivo was confirmed by using the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (C-PTIO), which blunted the responses to oral Nitrite. Our results showed that TEMPOL promotes Nitrite reduction to NO in the stomach and enhanced plasma Nitrite concentrations and the hypotensive effects of oral sodium Nitrite through mechanisms critically dependent on gastric pH. Interestingly, the effects of TEMPOL on Nitrite-mediated hypotension cannot be explained by increased NO formation in the stomach alone, but rather appear more directly related to increased plasma Nitrite levels and reduced nitrate levels during TEMPOL treatment. This may relate to enhanced Nitrite uptake or reduced nitrate formation from NO or Nitrite.

  • increase in gastric ph reduces hypotensive effect of oral sodium Nitrite in rats
    Free Radical Biology and Medicine, 2012
    Co-Authors: Lucas C Pinheiro, Jefferson H Amaral, Graziele C Ferreira, Marcelo F Montenegro, A Oliveira, Jose E Tanussantos

    Abstract The new pathway nitrateNitrite–nitric oxide (NO) has emerged as a physiological alternative to the classical enzymatic pathway for NO formation from l –arginine. Nitrate is converted to Nitrite by commensal bacteria in the oral cavity and the Nitrite formed is then swallowed and reduced to NO under the acidic conditions of the stomach. In this study, we tested the hypothesis that increases in gastric pH caused by omeprazole could decrease the hypotensive effect of oral sodium Nitrite. We assessed the effects of omeprazole treatment on the acute hypotensive effects produced by sodium Nitrite in normotensive and L-NAME-hypertensive free-moving rats. In addition, we assessed the changes in gastric pH and plasma levels of Nitrite, NO x (nitrate+Nitrite), and S -nitrosothiols caused by treatments. We found that the increases in gastric pH induced by omeprazole significantly reduced the hypotensive effects of sodium Nitrite in both normotensive and L-NAME-hypertensive rats. This effect of omeprazole was associated with no significant differences in plasma Nitrite, NO x , or S -nitrosothiol levels. Our results suggest that part of the hypotensive effects of oral sodium Nitrite may be due to its conversion to NO in the acidified environment of the stomach. The increase in gastric pH induced by treatment with omeprazole blunts part of the beneficial cardiovascular effects of dietary nitrate and Nitrite.

Enea Pagliano – One of the best experts on this subject based on the ideXlab platform.

  • high precision quadruple isotope dilution method for simultaneous determination of Nitrite and nitrate in seawater by gcms after derivatization with triethyloxonium tetrafluoroborate
    Analytica Chimica Acta, 2014
    Co-Authors: Enea Pagliano, Juris Meija, Zoltan Mester

    Abstract Quadruple isotope dilution mass spectrometry (ID 4 MS) has been applied for simultaneous determination of Nitrite and nitrate in seawater. ID 4 MS allows high-precision measurements and entails the use of isotopic internal standards ( 18 O-Nitrite and 15 N-nitrate). We include a tutorial on ID 4 MS outlining optimal experimental design which generates results with low uncertainties and obviates the need for direct (separate) evaluation of the procedural blank. Nitrite and nitrate detection was achieved using a headspace GCMS procedure based on single-step aqueous derivatization with triethyloxonium tetrafluoroborate at room temperature. In this paper the sample preparation was revised and fundamental aspects of this chemistry are presented. The proposed method has detection limits in the low parts-per-billion for both analytes, is reliable, precise, and has been validated using a seawater certified reference material (MOOS-2). Simplicity of the experimental design, low detection limits, and the use of quadruple isotope dilution makes the present method superior to the state-of-the-art for determination of Nitrite and nitrate, and an ideal candidate for reference measurements of these analytes in seawater.

  • quantification of Nitrite and nitrate in seawater by triethyloxonium tetrafluoroborate derivatization headspace spme gc ms
    Talanta, 2011
    Co-Authors: Enea Pagliano, Massimo Onor, Emanuela Pitzalis, Zoltan Mester, Ralph E. Sturgeon, Alessandro Dulivo

    Abstract Triethyloxonium tetrafluoroborate derivatization combined with direct headspace (HS) or SPME-gas chromatography–mass spectrometry (GC–MS) is proposed here for the simultaneous determination of Nitrite and nitrate in seawater at micromolar level after conversion to their corresponding volatile ethyl-esters (EtO-NO and EtO-NO2). Isotopically enriched Nitrite [15N] and nitrate [15N] are employed as internal standards and for quantification purposes. HS-GC–MS provided instrumental detection limits of 0.07 μM NO2− and 2 μM NO3−. Validation of the methodology was achieved by determination of Nitrite and nitrate in MOOS-1 (Seawater Certified Reference Material for Nutrients, NRC Canada), yielding results in excellent agreement with certified values. All critical aspects connected with the potential inter-conversion between Nitrite and nitrate (less than 10%) were evaluated and corrected for by the use of the isotopically enriched internal standard.

F Gotz – One of the best experts on this subject based on the ideXlab platform.