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Apocynin improves exercise performance and functional vasodilation by improving KATP function in obese Zucker rats
Author(s) -
Lu Silu,
Xiang Lusha,
Clemmer John,
Lee Lynn,
Sebai Mohamad,
Hester Robert L.
Publication year - 2012
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.26.1_supplement.860.17
Subject(s) - vasodilation , apocynin , glibenclamide , medicine , endocrinology , chemistry , vo2 max , nadph oxidase , oxidative stress , heart rate , diabetes mellitus , blood pressure
An impaired exercise performance and functional vasodilation has been observed in obesity. There is an increase in reactive oxygen species (ROS), which impairs functional vasodilation in obese Zucker rats (OZ), but the mechanism by which ROS impairs vascular function remains unclear. Since our laboratory has demonstrated that K ATP channel activation is required for functional vasodilation, we hypothesize that increased ROS would impair vascular K ATP channels in obesity, resulting in a blunted exercise capability. Ten‐week old lean Zucker rats (LZ) and OZ were treated with apocynin (drinking water, 2 mM) for five weeks. After the treatment, maximal oxygen consumption (VO 2max ) was measured during treadmill running with or without glibenclamide treatment (10 mg/kg, i.p.), a K ATP channel blocker. On the following day the spinotrapezius muscles were prepared for in vivo microscopy, with arcade arteriolar diameters being measured following muscle stimulation in the absence and presence of the glibenclamide (1 μM). OZ exhibited a significantly decreased VO 2max (42 ± 1 ml/kg/min) and functional vasodilation (34 ± 6%) as compared with LZ (VO 2max : 54 ± 1 ml/kg/min; vasodilation: 77 ± 2%). Apocynin treatment significantly increased VO 2max (45 ± 1 ml/kg/min) and functional vasodilation (64 ± 1%) in OZ with no effect in LZ. Glibenclamide significantly inhibited the VO 2max (46 ± 1 ml/kg/min) and functional vasodilation (39 ± 2%) in LZ and apocynin‐treated OZ (VO 2max : 41 ± 1 ml/kg/min; vasodilation: 35 ± 1%) but had no effect in control OZ. These results suggest that inhibition of ROS production by apocynin improves VO 2max and vascular function via improving impaired K ATP channel function in OZ. (Supported by NIH HL‐89581 and HL‐51971)