Format

Send to

Choose Destination
Microcirculation. 2017 Aug;24(6). doi: 10.1111/micc.12380.

Roles of NADPH oxidase and mitochondria in flow-induced vasodilation of human adipose arterioles: ROS-induced ROS release in coronary artery disease.

Author information

1
Cardiovascular Center, Department of Medicine, Medical College of Wisconsin, Milwaukee, WI, USA.
2
Department of Health and Medicine, Carroll University, Waukesha, WI, USA.
3
Department of Physical Therapy, Department of Medicine (Division of Pulmonary, Critical Care, Sleep and Allergy), University of Illinois at Chicago, Chicago, IL, USA.
4
Department of Physical Therapy, Department of Medicine (Division of Endocrinology, Diabetes and Metabolism), Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, IL, USA.

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.

KEYWORDS:

adipose; flow mediated dilation; microcirculation; mitochondria

PMID:
28480622
PMCID:
PMC5546408
DOI:
10.1111/micc.12380
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center