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Roles of NADPH oxidase and mitochondria in flow-induced vasodilation of human adipose arterioles: ROS-induced ROS release in coronary artery disease. Microcirculation 2017 Aug;24(6)

Date

05/10/2017

Pubmed ID

28480622

Pubmed Central ID

PMC5546408

DOI

10.1111/micc.12380

Scopus ID

2-s2.0-85026784719 (requires institutional sign-in at Scopus site)   33 Citations

Abstract

OBJECTIVES: H2 O2 contributes to FID of human arterioles. This study is designed to examine the roles of mitochondria and NADPH oxidase in modulating the release of ROS and in mediating FID. We tested whether NADPH oxidase contributes to mitochondrial ROS generation in arterioles during CAD.

METHODS: Visceral adipose arterioles obtained from patients with or without CAD were cannulated and pressurized for videomicroscopic measurement of arteriolar diameters. Dilator responses and ROS production during flow were determined in the presence and absence of the NADPH oxidase inhibitor gp91ds-tat and the mitochondrial electron transport inhibitor rotenone.

RESULTS: Both dilation and H2 O2 generation during flow were reduced in the presence of rotenone (13.5±8% vs 97±% without rotenone) or gp91ds-tat in patients with CAD, while patients without CAD exhibited H2 O2 -independent dilations. Mitochondrial superoxide production during flow was attenuated by gp91ds-tat in arterioles from CAD patients.

CONCLUSIONS: These findings indicate that ROS produced by NADPH oxidase are an upstream component of the mitochondria-dependent pathway contributing to flow-dependent H2 O2 generation and dilation in peripheral microvessels from patients with CAD. We conclude that in CAD, both mitochondria and NADPH oxidase contribute to FID through a redox mechanism in visceral arterioles.

Author List

Zinkevich NS, Fancher IS, Gutterman DD, Phillips SA

Author

Natalya S. Zinkevich PhD Research Scientist I in the Medicine department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Adipose Tissue
Arterioles
Coronary Artery Disease
Humans
Hydrogen Peroxide
Middle Aged
Mitochondria
NADPH Oxidases
Oxidation-Reduction
Reactive Oxygen Species
Vasodilation