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Decreased Large Conduit Artery Nitric Oxide Bioavailability in Metabolic Syndrome Effects Peripheral Microvessel Reactivity
Author(s) -
Branyan Kayla,
DeVallance Evan,
Lemaster Kent,
Skinner Roy,
Brooks Steve,
Asano Shinichi,
Willimas Justin,
Frisbee Jefferson,
Chantler Paul
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.729.6
Subject(s) - medicine , vasodilation , microvessel , nitric oxide , bioavailability , metabolic syndrome , arteriole , endothelial dysfunction , endocrinology , microcirculation , pharmacology , obesity , angiogenesis
One out of every five adults in the U.S. are considered to have multiple components of Metabolic Syndrome (MetS). These components include dyslipidemia, hypertension, insulin resistance, and a chronic pro‐inflammatory state, which significantly increase the risk for poor cardiovascular outcomes. Nitric oxide (NO) bioavailability is decreased in MetS, leading to vascular dysfunction. With this decrease in vascular function, there is an increased risk of poor cardiovascular outcomes. A common animal model used to mimic MetS is the obese Zucker rat (OZR) whereas its lean counterpart is used as a healthy control. The purpose of this study was to determine the extent of impairment in NO bioavailability in large conduit arteries and compare that to the reactivity of the related microvessels, such as the gracilis arteriole. Specifically, a DAF‐FM diacetate assay was used to determine the degree of NO production in the aorta. To assess microvessel reactivity, the gracilis arteriole was isolated, hung in a pressurized microvessel myobath, and was exposed to increasing doses of acetylcholine to measure endothelial function. TEMPOL was also used to determine the role of oxidant stress in modulating reactivity via vasodilation. LZRs had a higher overall NO bioavailability as compared to OZRs (p<0.05). This was reflected in gracilis reactivity where the LZRs had increased gracilis reactivity than OZRs overall (p<0.01). With TEMPOL, percent dilation was doubled in the gracilis of OZRs (p<0.01) but this effect was not seen in the LZRs. These results suggest that oxidant stress causes vascular dysfunction and that a higher NO bioavailability correlates with better microvascular reactivity. When a membrane‐permeable radical scavenger is introduced, reactive oxygen species that are causing the oxidative stress can be decreased to improve reactivity in a MetS model. Support or Funding Information AHA NIH