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Mechanisms of impaired acetylcholine‐mediated vasodilation in overweight rats
Author(s) -
Lekic Mateja,
Walker Benjimen R,
Sweazea Karen L
Publication year - 2010
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.24.1_supplement.592.3
Subject(s) - vasodilation , acetylcholine , sodium nitroprusside , medicine , endocrinology , nitric oxide , chemistry , mesenteric arteries , artery
The current study was designed to examine the early effects of increased adiposity in adult male Sprague‐Dawley rats fed either a high sucrose (HSD) or high fat diet (HFD) for 6 weeks. Initial studies examined pathways involved in acetylcholine (ACh)‐mediated vasodilation which is typically thought to act through increased production of the vasodilator nitric oxide (NO). Similar to obese animals, HSD and HFD‐fed rats developed impaired ACh‐mediated vasodilation in isolated mesenteric arteries compared to chow fed controls that was normalized by antioxidants. Unlike chow controls, inhibition of NO did not further impair vasodilation in the HSD or HFD groups suggesting that ACh may activate pathways distinct from NO in these settings. To examine smooth muscle sensitivity to NO, arteries were exposed to increasing concentrations of the NO donor sodium nitroprusside (10 −11 to 10 −3 M). We found that HSD and HFD reduced smooth muscle sensitivity to NO. These data suggest that increased ROS scavenging of NO coupled with diminished VSM reactivity minimizes the role of NO in vasodilation following HSD or HFD which is partially compensated by activation of parallel vasodilatory pathways.