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First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction

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First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction. / Wenzel, Philip; Mollnau, Hanke; Oelze, Matthias; Schulz, Eberhard; Wickramanayake, Jennifer M Dias; Müller, Johanna; Schuhmacher, Swenja; Hortmann, Marcus; Baldus, Stephan; Gori, Tommaso; Brandes, Ralf P; Münzel, Thomas; Daiber, Andreas.

In: ANTIOXID REDOX SIGN, Vol. 10, No. 8, 08.2008, p. 1435-1447.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Wenzel, P, Mollnau, H, Oelze, M, Schulz, E, Wickramanayake, JMD, Müller, J, Schuhmacher, S, Hortmann, M, Baldus, S, Gori, T, Brandes, RP, Münzel, T & Daiber, A 2008, 'First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction', ANTIOXID REDOX SIGN, vol. 10, no. 8, pp. 1435-1447. https://doi.org/10.1089/ars.2007.1969

APA

Wenzel, P., Mollnau, H., Oelze, M., Schulz, E., Wickramanayake, J. M. D., Müller, J., Schuhmacher, S., Hortmann, M., Baldus, S., Gori, T., Brandes, R. P., Münzel, T., & Daiber, A. (2008). First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction. ANTIOXID REDOX SIGN, 10(8), 1435-1447. https://doi.org/10.1089/ars.2007.1969

Vancouver

Wenzel P, Mollnau H, Oelze M, Schulz E, Wickramanayake JMD, Müller J et al. First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction. ANTIOXID REDOX SIGN. 2008 Aug;10(8):1435-1447. https://doi.org/10.1089/ars.2007.1969

Bibtex

@article{01fb0e1d798f4b1cb83d0d074bc7dfb2,
title = "First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction",
abstract = "Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revealing a dominant role of mitochondria for nitrate tolerance development. Isometric tension studies revealed that genetic deletion or inhibition (apocynin, 0.35 mg/h/4 day) of Nox improved ED, whereas nitrate tolerance was unaltered. Vice versa, nitrate tolerance was attenuated by co-treatment with the respiratory chain complex I inhibitor rotenone (100 microg/h/4 day) or the mitochondrial permeability transition pore blocker cyclosporine A (50 microg/h/4 day). Both compounds improved ED, suggesting a link between mitochondrial and Nox-derived ROS. Mitochondrial respiratory chain-derived ROS are critical for the development of nitrate tolerance, whereas Nox-derived ROS mediate nitrate tolerance-associated ED. This suggests a crosstalk between mitochondrial and Nox-derived ROS with distinct mechanistic effects and sites for pharmacological intervention.",
keywords = "Animals, Aorta/drug effects, Blotting, Western, Cell Line, Chromatography, High Pressure Liquid, Cyclosporine/administration & dosage, Ethidium/analogs & derivatives, Humans, In Vitro Techniques, Male, Mice, Mice, Inbred C57BL, Mitochondria, Heart/drug effects, NADPH Oxidases/genetics, Nitroglycerin/administration & dosage, RNA, Messenger/genetics, Rats, Rats, Wistar, Reactive Nitrogen Species/metabolism, Reactive Oxygen Species/metabolism, Reverse Transcriptase Polymerase Chain Reaction, Rotenone/administration & dosage, Transfection, Vasoconstriction/drug effects, Vasodilator Agents/administration & dosage",
author = "Philip Wenzel and Hanke Mollnau and Matthias Oelze and Eberhard Schulz and Wickramanayake, {Jennifer M Dias} and Johanna M{\"u}ller and Swenja Schuhmacher and Marcus Hortmann and Stephan Baldus and Tommaso Gori and Brandes, {Ralf P} and Thomas M{\"u}nzel and Andreas Daiber",
year = "2008",
month = aug,
doi = "10.1089/ars.2007.1969",
language = "English",
volume = "10",
pages = "1435--1447",
journal = "ANTIOXID REDOX SIGN",
issn = "1523-0864",
publisher = "Mary Ann Liebert Inc.",
number = "8",

}

RIS

TY - JOUR

T1 - First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction

AU - Wenzel, Philip

AU - Mollnau, Hanke

AU - Oelze, Matthias

AU - Schulz, Eberhard

AU - Wickramanayake, Jennifer M Dias

AU - Müller, Johanna

AU - Schuhmacher, Swenja

AU - Hortmann, Marcus

AU - Baldus, Stephan

AU - Gori, Tommaso

AU - Brandes, Ralf P

AU - Münzel, Thomas

AU - Daiber, Andreas

PY - 2008/8

Y1 - 2008/8

N2 - Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revealing a dominant role of mitochondria for nitrate tolerance development. Isometric tension studies revealed that genetic deletion or inhibition (apocynin, 0.35 mg/h/4 day) of Nox improved ED, whereas nitrate tolerance was unaltered. Vice versa, nitrate tolerance was attenuated by co-treatment with the respiratory chain complex I inhibitor rotenone (100 microg/h/4 day) or the mitochondrial permeability transition pore blocker cyclosporine A (50 microg/h/4 day). Both compounds improved ED, suggesting a link between mitochondrial and Nox-derived ROS. Mitochondrial respiratory chain-derived ROS are critical for the development of nitrate tolerance, whereas Nox-derived ROS mediate nitrate tolerance-associated ED. This suggests a crosstalk between mitochondrial and Nox-derived ROS with distinct mechanistic effects and sites for pharmacological intervention.

AB - Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revealing a dominant role of mitochondria for nitrate tolerance development. Isometric tension studies revealed that genetic deletion or inhibition (apocynin, 0.35 mg/h/4 day) of Nox improved ED, whereas nitrate tolerance was unaltered. Vice versa, nitrate tolerance was attenuated by co-treatment with the respiratory chain complex I inhibitor rotenone (100 microg/h/4 day) or the mitochondrial permeability transition pore blocker cyclosporine A (50 microg/h/4 day). Both compounds improved ED, suggesting a link between mitochondrial and Nox-derived ROS. Mitochondrial respiratory chain-derived ROS are critical for the development of nitrate tolerance, whereas Nox-derived ROS mediate nitrate tolerance-associated ED. This suggests a crosstalk between mitochondrial and Nox-derived ROS with distinct mechanistic effects and sites for pharmacological intervention.

KW - Animals

KW - Aorta/drug effects

KW - Blotting, Western

KW - Cell Line

KW - Chromatography, High Pressure Liquid

KW - Cyclosporine/administration & dosage

KW - Ethidium/analogs & derivatives

KW - Humans

KW - In Vitro Techniques

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Mitochondria, Heart/drug effects

KW - NADPH Oxidases/genetics

KW - Nitroglycerin/administration & dosage

KW - RNA, Messenger/genetics

KW - Rats

KW - Rats, Wistar

KW - Reactive Nitrogen Species/metabolism

KW - Reactive Oxygen Species/metabolism

KW - Reverse Transcriptase Polymerase Chain Reaction

KW - Rotenone/administration & dosage

KW - Transfection

KW - Vasoconstriction/drug effects

KW - Vasodilator Agents/administration & dosage

U2 - 10.1089/ars.2007.1969

DO - 10.1089/ars.2007.1969

M3 - SCORING: Journal article

C2 - 18522491

VL - 10

SP - 1435

EP - 1447

JO - ANTIOXID REDOX SIGN

JF - ANTIOXID REDOX SIGN

SN - 1523-0864

IS - 8

ER -