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Michael August

Researcher at University of Mainz

Publications -  10
Citations -  1801

Michael August is an academic researcher from University of Mainz. The author has contributed to research in topics: Superoxide & Nitric oxide. The author has an hindex of 10, co-authored 10 publications receiving 1727 citations. Previous affiliations of Michael August include University of Hamburg.

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Effects of Angiotensin II Infusion on the Expression and Function of NAD(P)H Oxidase and Components of Nitric Oxide/cGMP Signaling

TL;DR: It is concluded that angiotensin II-induced increases in the activity and the expression of NAD(P)H oxidase are at least in part PKC-dependent and may trigger NOS III uncoupling, leading to impaired NO/cGMP signaling and to endothelial dysfunction in this animal model.
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Central role of mitochondrial aldehyde dehydrogenase and reactive oxygen species in nitroglycerin tolerance and cross-tolerance

TL;DR: Nitrate tolerance is mediated, at least in significant part, by inhibition of vascular ALDH-2 and that mitochondrial ROS contribute to this inhibition, and GTN tolerance may be viewed as a metabolic syndrome characterized by mitochondrial dysfunction.
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Measurement of NAD(P)H oxidase-derived superoxide with the luminol analogue L-012.

TL;DR: Experiments using electron paramagnetic resonance and the spin trap 5-diethoxyphosphoryl-5-methyl-1-pyrroline-N-oxide revealed that in contrast to lucigenin, L-012 is not subject to redox cycling.
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Reversal of Endothelial Nitric Oxide Synthase Uncoupling and Up-Regulation of Endothelial Nitric Oxide Synthase Expression Lowers Blood Pressure in Hypertensive Rats

TL;DR: Pharmacologic interventions that combine eNOS up-regulation and reversal of eN OS uncoupling can markedly increase bioactive NO in the vasculature and produce beneficial hemodynamic effects such as a reduction of blood pressure.
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Nebivolol Prevents Vascular NOS III Uncoupling in Experimental Hyperlipidemia and Inhibits NADPH Oxidase Activity in Inflammatory Cells

TL;DR: Nebivolol therapy effectively prevents NO synthase III uncoupling and prevents activation of the neutrophil NAD(P)H oxidase and infiltration of inflammatory cells, which may explain partly the beneficial effects on endothelial function in patients with enhanced vascular oxidative stress.