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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:791.)
© 2007 American Heart Association, Inc.

Vascular Biology

Exercise Training Restores Coronary Arteriolar Dilation to NOS Activation Distal to Coronary Artery Occlusion

Role of Hydrogen Peroxide

Naris Thengchaisri; Robert Shipley; Yi Ren; Janet Parker; Lih Kuo

From the Department of Systems Biology and Translational Medicine, Cardiovascular Research Institute, College of Medicine, Texas A&M Health Science Center, Temple, Tex. Current address for N.T.: Faculty of Veterinary Medicine, Kasetsart University, 50 Paholyothin Road, Bangkhen, Bangkok 10900, Thailand.

Correspondence to Lih Kuo, PhD, Department of Systems Biology and Translational Medicine, Cardiovascular Research Institute, College of Medicine, Texas A&M Health Science Center, 702 Southwest H.K. Dodgen Loop, Temple, TX 76504. E-mail LKUO{at}tamu.edu

Objective— Exercise training has been shown to restore vasodilation to nitric oxide synthase (NOS) activation in arterioles distal to coronary artery occlusion. Because reactive oxygen species are generated during NOS uncoupling and the production of vasodilator H₂O₂ is increased during exercise in patients with coronary disease, we proposed that H₂O₂ may contribute to the restoration of vasodilation in porcine coronary occlusion model.

Methods and Results— Left circumflex (LCX) coronary artery of miniature swine was progressively occluded for 8 weeks followed by exercise training (EX; 5 days/wk treadmill) or sedentary (SED) protocols for 12 weeks. Arterioles were isolated from distal LCX and nonoccluded left anterior descending (LAD) artery for in vitro study. Vasodilation to NOS activators adenosine and ionomycin was impaired in SED LCX, but not LAD, arterioles. This impairment was restored by L-arginine. NO production induced by adenosine was also reduced in SED LCX arterioles. EX had no effect on LAD arterioles but improved NO production and restored dilation of LCX arterioles. NOS blockade (L-NAME) inhibited vasodilation to NOS activators in LAD (SED & EX) arterioles but was ineffective in SED LCX arterioles. In EX LCX arterioles, vasodilation to NOS activators was slightly inhibited by L-NAME but abolished by catalase. H₂O₂ production was markedly increased by adenosine in EX LCX arterioles.

Conclusions— This study demonstrates that endothelium-dependent NO-mediated dilation is impaired in SED LCX arterioles and that EX training restores the impaired function. It appears that H₂O₂, in addition to NO, contributes significantly to EX-induced restoration of endothelium-dependent dilation of coronary arterioles distal to occlusion.

This study demonstrates that endothelium-dependent NO-mediated dilation is impaired in SED LCX arterioles and that EX training restores the impaired function. It appears that H₂O₂, in addition to NO, contributes significantly to EX-induced restoration of endothelium-dependent dilation of coronary arterioles distal to occlusion.

Key Words: nitric oxide • vasodilation • collateral circulation • hydrogen peroxide • L-arginine