Premium
Aerobic Exercise Dampens Acute Hypertension‐Induced Vascular Oxidative Stress
Author(s) -
Robinson Austin T,
Fancher Ibra Seaphus,
Bian JingTan,
Ali Mohamed M,
Sudhahar Varadarajan,
UshioFukai Masuko,
Fukai Tohru,
Levitan Irena,
Phillips Shane A
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.763.27
Subject(s) - apocynin , losartan , nadph oxidase , medicine , oxidative stress , endocrinology , nitric oxide synthase , nitric oxide , aerobic exercise , angiotensin ii , chemistry , blood pressure
Regular exercise prevents endothelium dysfunction (ED) following acute strenuous physical exertion. Acute strenuous exertion induces ED via exposing the vascular endothelium to transient hypertension (HTN). The purpose of this study was to determine the mechanisms through which regular exercise may protect the endothelium against HTN‐induced ED. Twenty‐eight 14–18 week mice were assigned to voluntary wheel running for two weeks (EX; mean: 7 miles/day) or control (CON). Hind limb subcutaneous adipose resistance arteries (RAs) were dissected and cannulated for measures of flow induced dilation (FID) with and without exposure to high intraluminal pressure (HILP; 110mmHg) and pharmacological agents including the nitric oxide synthase (NOS) inhibitor L‐NAME (100 μM), hydrogen peroxide (H 2 O 2 ) scavenger PEG‐Cat (500 U/ml, and the angiotensin receptor blocker losartan (10 μM). Fluorescence microscopy was used to determine O 2 − and H 2 O 2 production and western blot was used to determine NOX2 and SOD content. Following exposure to acute HILP, FID was preserved in EX and reduced in CON but rescued with losartan, NADPH oxidase inhibition (VAS2870; 2 μM) and the anti‐oxidant Apocynin (50 μM). Furthermore, preserved FID in EX was significantly reduced in the presence of PEG‐Cat compared to L‐NAME. CON expressed more NOX2 and produced greater amounts of O 2 − following transient HTN while EX expressed more SOD and produced more H 2 O 2. These findings suggest regular exercise prevents HTN‐induced reductions in FID and the mechanism involves attenuating RAAS activation of NOX2 generation and dismutation of O 2 − to H 2 O 2 . Support or Funding Information NHLBI K23HL85614, RO1HL095701, and HL095701‐01A2S